786 o cells  (ATCC)


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    Structured Review

    ATCC 786 o cells
    a Structures of itaconate, isomers and octyl-derivatives b <t>786-O</t> cells pretreated with octyl-derivatives (80 μM) or metabolites (25 mM) for 24 h, then infected with VSVΔ51 (MOI of 0.01). Virus-infected cells quantified by flow cytometry at 17 h post-infection. c Flow cytometry analysis of virus-infected cells in 786-O cells treated with increasing 4-OI concentrations at 17 h post-infection. d Host vs viral RNA ratio in VSVΔ51-infected 786-O cells (MOI of 0.01) with or without 4-OI (75 μM). e – g Cancer lines pretreated with 4-OI (125 μM or 75 μM for 786-O cells) for 24 h, then infected with VSVΔ51 at varying MOIs. Viral titers determined from supernatants 24 h post-infection. h 786-O cells pretreated with 4-OI (75 μM) for 24 h and infected with VSVΔ51 (MOI of 0.0001), followed by plaque imaging. Scale bars, 200 μm. i Plaque diameters measured 24 h after infection. j 786-O cellular layer integrity assessed by Calcein green staining after treatment with 4-OI (75 μM) and VSVΔ51 infection (MOI 0.01) for 24 h. Scale bars, 100 μm. k CT26WT cells treated with 4-OI (125 μM) for 24 h post-infection with VSVΔ51 (MOI 0.01) for 48 h. Cleaved caspase 3 in cyan blue, nuclei in dark blue stained with DAPI, and actin filaments with phalloidin in green. Scale bars, 100 μm. l , m CT26WT and 786-O cells pretreated with 4-OI (125 μM) and (75 μM), respectively, for 24 h, then infected with VSVΔ51 at a MOI of 0.01. Percentage of viable cells determined by flow cytometry at 30 h post-infection. Data are means ± SEM of two independent experiments in duplicates in ( b , c , e – g ) (except for CT26WT and 76-9, from one experiment in triplicates); one experiment in triplicates for ( d ); one experiment in multiple replicates for ( I ); and two experiments in triplicates for ( l , m ). Images are from one experiment in ( h ), one representative experiment out of two in ( j ), and one out of two in ( k ). Statistical significance indicated by one-way ANOVA for ( b , c , l , m ); and two-tailed Student’s t -test for ( e – g , i ). Source data provided in a Source Data file.
    786 O Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/786 o cells/product/ATCC
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    786 o cells - by Bioz Stars, 2024-05
    86/100 stars

    Images

    1) Product Images from "Octyl itaconate enhances VSVΔ51 oncolytic virotherapy by multitarget inhibition of antiviral and inflammatory pathways"

    Article Title: Octyl itaconate enhances VSVΔ51 oncolytic virotherapy by multitarget inhibition of antiviral and inflammatory pathways

    Journal: Nature Communications

    doi: 10.1038/s41467-024-48422-x

    a Structures of itaconate, isomers and octyl-derivatives b 786-O cells pretreated with octyl-derivatives (80 μM) or metabolites (25 mM) for 24 h, then infected with VSVΔ51 (MOI of 0.01). Virus-infected cells quantified by flow cytometry at 17 h post-infection. c Flow cytometry analysis of virus-infected cells in 786-O cells treated with increasing 4-OI concentrations at 17 h post-infection. d Host vs viral RNA ratio in VSVΔ51-infected 786-O cells (MOI of 0.01) with or without 4-OI (75 μM). e – g Cancer lines pretreated with 4-OI (125 μM or 75 μM for 786-O cells) for 24 h, then infected with VSVΔ51 at varying MOIs. Viral titers determined from supernatants 24 h post-infection. h 786-O cells pretreated with 4-OI (75 μM) for 24 h and infected with VSVΔ51 (MOI of 0.0001), followed by plaque imaging. Scale bars, 200 μm. i Plaque diameters measured 24 h after infection. j 786-O cellular layer integrity assessed by Calcein green staining after treatment with 4-OI (75 μM) and VSVΔ51 infection (MOI 0.01) for 24 h. Scale bars, 100 μm. k CT26WT cells treated with 4-OI (125 μM) for 24 h post-infection with VSVΔ51 (MOI 0.01) for 48 h. Cleaved caspase 3 in cyan blue, nuclei in dark blue stained with DAPI, and actin filaments with phalloidin in green. Scale bars, 100 μm. l , m CT26WT and 786-O cells pretreated with 4-OI (125 μM) and (75 μM), respectively, for 24 h, then infected with VSVΔ51 at a MOI of 0.01. Percentage of viable cells determined by flow cytometry at 30 h post-infection. Data are means ± SEM of two independent experiments in duplicates in ( b , c , e – g ) (except for CT26WT and 76-9, from one experiment in triplicates); one experiment in triplicates for ( d ); one experiment in multiple replicates for ( I ); and two experiments in triplicates for ( l , m ). Images are from one experiment in ( h ), one representative experiment out of two in ( j ), and one out of two in ( k ). Statistical significance indicated by one-way ANOVA for ( b , c , l , m ); and two-tailed Student’s t -test for ( e – g , i ). Source data provided in a Source Data file.
    Figure Legend Snippet: a Structures of itaconate, isomers and octyl-derivatives b 786-O cells pretreated with octyl-derivatives (80 μM) or metabolites (25 mM) for 24 h, then infected with VSVΔ51 (MOI of 0.01). Virus-infected cells quantified by flow cytometry at 17 h post-infection. c Flow cytometry analysis of virus-infected cells in 786-O cells treated with increasing 4-OI concentrations at 17 h post-infection. d Host vs viral RNA ratio in VSVΔ51-infected 786-O cells (MOI of 0.01) with or without 4-OI (75 μM). e – g Cancer lines pretreated with 4-OI (125 μM or 75 μM for 786-O cells) for 24 h, then infected with VSVΔ51 at varying MOIs. Viral titers determined from supernatants 24 h post-infection. h 786-O cells pretreated with 4-OI (75 μM) for 24 h and infected with VSVΔ51 (MOI of 0.0001), followed by plaque imaging. Scale bars, 200 μm. i Plaque diameters measured 24 h after infection. j 786-O cellular layer integrity assessed by Calcein green staining after treatment with 4-OI (75 μM) and VSVΔ51 infection (MOI 0.01) for 24 h. Scale bars, 100 μm. k CT26WT cells treated with 4-OI (125 μM) for 24 h post-infection with VSVΔ51 (MOI 0.01) for 48 h. Cleaved caspase 3 in cyan blue, nuclei in dark blue stained with DAPI, and actin filaments with phalloidin in green. Scale bars, 100 μm. l , m CT26WT and 786-O cells pretreated with 4-OI (125 μM) and (75 μM), respectively, for 24 h, then infected with VSVΔ51 at a MOI of 0.01. Percentage of viable cells determined by flow cytometry at 30 h post-infection. Data are means ± SEM of two independent experiments in duplicates in ( b , c , e – g ) (except for CT26WT and 76-9, from one experiment in triplicates); one experiment in triplicates for ( d ); one experiment in multiple replicates for ( I ); and two experiments in triplicates for ( l , m ). Images are from one experiment in ( h ), one representative experiment out of two in ( j ), and one out of two in ( k ). Statistical significance indicated by one-way ANOVA for ( b , c , l , m ); and two-tailed Student’s t -test for ( e – g , i ). Source data provided in a Source Data file.

    Techniques Used: Infection, Virus, Flow Cytometry, Imaging, Staining, Two Tailed Test

    a NRF2 protein levels in control and NRF2 knockout (KO) 786-O cells treated with 4-OI (75 μM) for 24 h using confocal microscopy. Blue: actin filaments, green: NRF2. Scale bars, 50 μm. b KEAP1 levels analyzed in 786-O cells treated with alkynated 4-OI (4-OI-alk) (125 μM) for 4 or 24 h with or without non-alkynated 4-OI (125 μM) by anti-KEAP1 immunoblotting. c Viral RNA content assessed by RNA sequencing in VSVΔ51-infected (MOI of 0.01) control and NRF2 KO 786-O cells with or without 4-OI (75 μM) pretreatment. d – f Immunoblot analysis in control and NRF2 KO cells pretreated with 4-OI (75 μM) before VSVΔ51 challenge (MOI of 0.01) ( d ). Fluorescence microscopy showing VSVΔ51-RFP spread and cellular layer integrity with Hoechst stain overlay (Scale bars, 300 μm) ( e ) and quantification of infected cells by flow cytometry at 17 h post-infection ( f ). g – j Quantification of virus-infected cells by flow cytometry in 786-O cells transiently KO for NRF2 ( g ) or KEAP1 ( j ). Immunoblot analysis in NRF2 KO ( h ) and KEAP1 KO cells ( i ) pretreated with 4-OI (75 μM) before VSVΔ51 challenge (MOI of 0.01). k 786-O cells incubated with L-NAC (1 mM) for 3 h before 4-OI challenge (75 μM) for 24 h, then infected with VSVΔ51-RFP (MOI of 0.01). Quantification of infected cells by flow cytometry at 17 h post-infection. Data are means ± SEM from two independent experiments in biological duplicates and triplicates in ( f ), and in biological triplicates and quadruplicates in ( g ). Two experiments in biological quadruplicates in ( j ) and ( k ). Images from one representative experiment in triplicates in ( a ) and ( e ). Data in ( b ) and ( d ) from one representative of three independent experiments. Data as means ± SEM from one experiment in biological triplicates in ( c ). Statistics indicate significance by one-way ANOVA for ( f , g , j , k ). Vertical stacks of bands are not derived from the same membrane in ( d , h , I ). Source data provided in the Source Data file.
    Figure Legend Snippet: a NRF2 protein levels in control and NRF2 knockout (KO) 786-O cells treated with 4-OI (75 μM) for 24 h using confocal microscopy. Blue: actin filaments, green: NRF2. Scale bars, 50 μm. b KEAP1 levels analyzed in 786-O cells treated with alkynated 4-OI (4-OI-alk) (125 μM) for 4 or 24 h with or without non-alkynated 4-OI (125 μM) by anti-KEAP1 immunoblotting. c Viral RNA content assessed by RNA sequencing in VSVΔ51-infected (MOI of 0.01) control and NRF2 KO 786-O cells with or without 4-OI (75 μM) pretreatment. d – f Immunoblot analysis in control and NRF2 KO cells pretreated with 4-OI (75 μM) before VSVΔ51 challenge (MOI of 0.01) ( d ). Fluorescence microscopy showing VSVΔ51-RFP spread and cellular layer integrity with Hoechst stain overlay (Scale bars, 300 μm) ( e ) and quantification of infected cells by flow cytometry at 17 h post-infection ( f ). g – j Quantification of virus-infected cells by flow cytometry in 786-O cells transiently KO for NRF2 ( g ) or KEAP1 ( j ). Immunoblot analysis in NRF2 KO ( h ) and KEAP1 KO cells ( i ) pretreated with 4-OI (75 μM) before VSVΔ51 challenge (MOI of 0.01). k 786-O cells incubated with L-NAC (1 mM) for 3 h before 4-OI challenge (75 μM) for 24 h, then infected with VSVΔ51-RFP (MOI of 0.01). Quantification of infected cells by flow cytometry at 17 h post-infection. Data are means ± SEM from two independent experiments in biological duplicates and triplicates in ( f ), and in biological triplicates and quadruplicates in ( g ). Two experiments in biological quadruplicates in ( j ) and ( k ). Images from one representative experiment in triplicates in ( a ) and ( e ). Data in ( b ) and ( d ) from one representative of three independent experiments. Data as means ± SEM from one experiment in biological triplicates in ( c ). Statistics indicate significance by one-way ANOVA for ( f , g , j , k ). Vertical stacks of bands are not derived from the same membrane in ( d , h , I ). Source data provided in the Source Data file.

    Techniques Used: Knock-Out, Confocal Microscopy, Western Blot, RNA Sequencing Assay, Infection, Fluorescence, Microscopy, Staining, Flow Cytometry, Virus, Incubation, Derivative Assay, Membrane

    a – c 786-O cells pretreated with 4-OI (75 μM) for 24 h and infected with VSVΔ51 (MOI 0.01) for 17 h. RNA sequencing analysis emphasizing on antiviral genes (blue dots) in the volcano plot ( a ), differentially expressed interferon-stimulated genes (ISGs) in the heat map ( b ), and top KEGG pathways affected by 4-OI during viral infection (one-sided hypergeometric test, Benjamini–Hochberg method was applied to adjust the p -value for multiple testing) ( c ). d , e 786-O cells pretreated with 4-OI (125 μM) for 24 h and infected with VSVΔ51-RFP (MOI 0.01) for 24 h. IFIT1 levels assessed by fluorescence microscopy ( d ), and Western blot performed on cell lysates for antiviral proteins ( e ). f 786-O cells pretreated with 4-OI (75 μM) for 24 h infected with wild-type VSV (wt VSV) or VSVΔ51 at MOI 0.01. Viral titers determined 24 h post-infection. g – i Control and NRF2 KO 786-O cells, as well as 786-O cells transiently KO for NRF2 or KEAP using CRISPR/Cas9, pretreated with 4-OI (75 μM) for 24 h and infected with VSVΔ51 (MOI 0.01) for 17 h. Immunoblots in ( g , h ). CXCL10 release measured by ELISA from supernatants in ( I ). j Control and NRF2 KO 786-O cells pretreated with 4-OI (75 μM) for 24 h and stimulated with the RIG-I agonist M8 (3.5 ng/mL) for 5 h. Western blot performed on cell lysates. Data are from one experiment performed in triplicate in ( a – c ). Images are from one experiment in ( d ). Data are from one representative experiment performed at least three times in ( e ). Data are depicted as means ± SEM from one experiment performed in triplicate in ( f ). Data are from one representative experiment out of three in ( g ), out of two in ( h ) and ( j ). Data are depicted as means ± SEM from two experiments performed in triplicate in ( I ). Statistics indicate significance by two-way ANOVA for ( f , I ). Vertical stacks of bands are not derived from the same membrane in ( e , g , h , j ). Source data provided as a Source Data file.
    Figure Legend Snippet: a – c 786-O cells pretreated with 4-OI (75 μM) for 24 h and infected with VSVΔ51 (MOI 0.01) for 17 h. RNA sequencing analysis emphasizing on antiviral genes (blue dots) in the volcano plot ( a ), differentially expressed interferon-stimulated genes (ISGs) in the heat map ( b ), and top KEGG pathways affected by 4-OI during viral infection (one-sided hypergeometric test, Benjamini–Hochberg method was applied to adjust the p -value for multiple testing) ( c ). d , e 786-O cells pretreated with 4-OI (125 μM) for 24 h and infected with VSVΔ51-RFP (MOI 0.01) for 24 h. IFIT1 levels assessed by fluorescence microscopy ( d ), and Western blot performed on cell lysates for antiviral proteins ( e ). f 786-O cells pretreated with 4-OI (75 μM) for 24 h infected with wild-type VSV (wt VSV) or VSVΔ51 at MOI 0.01. Viral titers determined 24 h post-infection. g – i Control and NRF2 KO 786-O cells, as well as 786-O cells transiently KO for NRF2 or KEAP using CRISPR/Cas9, pretreated with 4-OI (75 μM) for 24 h and infected with VSVΔ51 (MOI 0.01) for 17 h. Immunoblots in ( g , h ). CXCL10 release measured by ELISA from supernatants in ( I ). j Control and NRF2 KO 786-O cells pretreated with 4-OI (75 μM) for 24 h and stimulated with the RIG-I agonist M8 (3.5 ng/mL) for 5 h. Western blot performed on cell lysates. Data are from one experiment performed in triplicate in ( a – c ). Images are from one experiment in ( d ). Data are from one representative experiment performed at least three times in ( e ). Data are depicted as means ± SEM from one experiment performed in triplicate in ( f ). Data are from one representative experiment out of three in ( g ), out of two in ( h ) and ( j ). Data are depicted as means ± SEM from two experiments performed in triplicate in ( I ). Statistics indicate significance by two-way ANOVA for ( f , I ). Vertical stacks of bands are not derived from the same membrane in ( e , g , h , j ). Source data provided as a Source Data file.

    Techniques Used: Infection, RNA Sequencing Assay, Fluorescence, Microscopy, Western Blot, CRISPR, Enzyme-linked Immunosorbent Assay, Derivative Assay, Membrane

    a HEK293 cells pretreated with increasing 4-OI concentrations (75 and 125 μM) and transfected with GFP-tagged plasmids. Immunoblotting analyzes antiviral proteins. b , c Data from Runtsch et al. . THP1 cells treated with 4-OI (125 μM), prior challenge with IA-DTB, cell lysis, and measurement of modified cysteines by LC-MS. d 786-O cells treated with 125 μM of 4-OI-alk (4 or 24 h) with or without 4-OI (125 μM), followed by click chemistry and biotin enrichment. Samples before and after enrichment analyzed by anti-MAVS immunoblotting. e HEK293 cells pretreated or not with 4-OI (125 μM) and transfected with Flag-tagged MAVS together with GFP-tagged RIG-I or TBK1 as indicated. Whole-cell extracts prepared and immunoprecipitated with anti-Flag antibody M2; immunoprecipitated complexes or 5% input run on SDS-PAGE and probed with anti-GFP/anti-Flag antibodies. f , g Transient MAVS KO 786-O cells treated with 4-OI, then infected with VSVΔ51, analyzed by Western blot ( f ) and flow cytometry ( g ). h HEK293 cells transfected with a plasmid encoding Flag-tagged MAVS wt or mutant Flag-tagged MAVS C283A for 24 h. Subsequently, cells treated with 125 μM of alkynated 4-OI (4-OI-alk) for 4 h, followed by click chemistry and biotin enrichment. Samples before and after enrichment analyzed by anti-Flag immunoblotting. i HEK293 cells stimulated with 4-OI prior to transfection with MAVS wt or mutant C283A MAVS, analyzed by ISRE promoter luciferase activity. j HEK293 cells transfected with MAVS wt or mutant together with TBK1, treated with 4-OI, analyzed by immunoprecipitation and immunoblotting. Data from one representative experiment in ( a ), three independent experiments in ( b , c ), one representative experiment performed three times in ( d ), one experiment in ( e , h , j ). Data from one representative experiment out of two in ( f ). Data depicted as means ± SEM from two independent experiments performed in triplicates and quadruplicates in ( g ), two independent experiments in triplicates in ( I ). Statistical significance by one-way ANOVA for ( g ) and two-way ANOVA for ( I ). Vertical stacks of bands are not derived from the same membrane in ( a , e , f , j ). Source data provided in Source Data file.
    Figure Legend Snippet: a HEK293 cells pretreated with increasing 4-OI concentrations (75 and 125 μM) and transfected with GFP-tagged plasmids. Immunoblotting analyzes antiviral proteins. b , c Data from Runtsch et al. . THP1 cells treated with 4-OI (125 μM), prior challenge with IA-DTB, cell lysis, and measurement of modified cysteines by LC-MS. d 786-O cells treated with 125 μM of 4-OI-alk (4 or 24 h) with or without 4-OI (125 μM), followed by click chemistry and biotin enrichment. Samples before and after enrichment analyzed by anti-MAVS immunoblotting. e HEK293 cells pretreated or not with 4-OI (125 μM) and transfected with Flag-tagged MAVS together with GFP-tagged RIG-I or TBK1 as indicated. Whole-cell extracts prepared and immunoprecipitated with anti-Flag antibody M2; immunoprecipitated complexes or 5% input run on SDS-PAGE and probed with anti-GFP/anti-Flag antibodies. f , g Transient MAVS KO 786-O cells treated with 4-OI, then infected with VSVΔ51, analyzed by Western blot ( f ) and flow cytometry ( g ). h HEK293 cells transfected with a plasmid encoding Flag-tagged MAVS wt or mutant Flag-tagged MAVS C283A for 24 h. Subsequently, cells treated with 125 μM of alkynated 4-OI (4-OI-alk) for 4 h, followed by click chemistry and biotin enrichment. Samples before and after enrichment analyzed by anti-Flag immunoblotting. i HEK293 cells stimulated with 4-OI prior to transfection with MAVS wt or mutant C283A MAVS, analyzed by ISRE promoter luciferase activity. j HEK293 cells transfected with MAVS wt or mutant together with TBK1, treated with 4-OI, analyzed by immunoprecipitation and immunoblotting. Data from one representative experiment in ( a ), three independent experiments in ( b , c ), one representative experiment performed three times in ( d ), one experiment in ( e , h , j ). Data from one representative experiment out of two in ( f ). Data depicted as means ± SEM from two independent experiments performed in triplicates and quadruplicates in ( g ), two independent experiments in triplicates in ( I ). Statistical significance by one-way ANOVA for ( g ) and two-way ANOVA for ( I ). Vertical stacks of bands are not derived from the same membrane in ( a , e , f , j ). Source data provided in Source Data file.

    Techniques Used: Transfection, Western Blot, Lysis, Modification, Liquid Chromatography with Mass Spectroscopy, Immunoprecipitation, SDS Page, Infection, Flow Cytometry, Plasmid Preparation, Mutagenesis, Luciferase, Activity Assay, Derivative Assay, Membrane

    a CiiiDER analysis to identify overrepresented transcription factor binding sites in 786-O cells treated or not with 4-OI (75 µM) prior VSVΔ51 (MOI 0.01 for 17 h). b , c Confocal microscopy of p65 nuclear translocation in 786-O cells treated or not with 4-OI following VSVΔ51 (Scale, 20 μm) ( b ); IL-6 levels measured by ELISA ( c ). d , e Data from Runtsch et al. . THP1 cells treated with 4-OI following IA-DTB, cell lysis, and LC-MS measurements of modified cysteines. f 786-O cells upon 4-OI-alk with or without 4-OI (both 125 µM). Immunoblotting of IKKβ, IKKγ, and IKK ε before and after biotin enrichment. g Illustration of 4-OI binding (green) to IKKβ at Cys179 (left) and 2D ligand-protein interactions (right). Lipophilicity protein surface: lipophilic (cyan), hydrophilic (violet), neutral (white), α-helices (cyan), β-sheets (yellow), loops (cyan). h Luciferase NF-kB promotor activity in control and NRF2 KO 786-O treated or not with 4-OI prior to control (pc) or IKKβ plasmid transfection. i Immunoblotting of IKKα/β, IκBα, and P65 phosphorylation in 786-O cells treated or not with 4-OI prior VSVΔ51. j , k IKKβ KO 786-O cells treated or not with 4-OI following VSVΔ51, immunoblotting ( j ) and flow ( k ) analyses. l Luciferase assay of NF-κB promotor activity in HEK293 cells stimulated or not with 4-OI prior to IKKβ wt or IKKβ C179A plasmid transfection. Data from one representative experiment in ( a ), two independent experiments in ( b ). Data are depicted as means ± SEM from two experiments in triplicates in ( c ), three independent experiments in ( d , e ). Data from one representative experiment out of three in ( f ). Data are depicted as means from one experiment in duplicates in ( h ). Data from one representative experiment performed twice in ( I , j ). Data are the means ± SEM from two experiments performed in quadruplicates in ( k ). Data are the means ± SEM from two experiments in triplicates in ( l ). Statistical significance by two-way ANOVA for ( c , l ) and one-way ANOVA for ( k ). Vertical stacks of bands are not derived from the same membrane in ( f , i , j ). Source data are provided in Source Data file.
    Figure Legend Snippet: a CiiiDER analysis to identify overrepresented transcription factor binding sites in 786-O cells treated or not with 4-OI (75 µM) prior VSVΔ51 (MOI 0.01 for 17 h). b , c Confocal microscopy of p65 nuclear translocation in 786-O cells treated or not with 4-OI following VSVΔ51 (Scale, 20 μm) ( b ); IL-6 levels measured by ELISA ( c ). d , e Data from Runtsch et al. . THP1 cells treated with 4-OI following IA-DTB, cell lysis, and LC-MS measurements of modified cysteines. f 786-O cells upon 4-OI-alk with or without 4-OI (both 125 µM). Immunoblotting of IKKβ, IKKγ, and IKK ε before and after biotin enrichment. g Illustration of 4-OI binding (green) to IKKβ at Cys179 (left) and 2D ligand-protein interactions (right). Lipophilicity protein surface: lipophilic (cyan), hydrophilic (violet), neutral (white), α-helices (cyan), β-sheets (yellow), loops (cyan). h Luciferase NF-kB promotor activity in control and NRF2 KO 786-O treated or not with 4-OI prior to control (pc) or IKKβ plasmid transfection. i Immunoblotting of IKKα/β, IκBα, and P65 phosphorylation in 786-O cells treated or not with 4-OI prior VSVΔ51. j , k IKKβ KO 786-O cells treated or not with 4-OI following VSVΔ51, immunoblotting ( j ) and flow ( k ) analyses. l Luciferase assay of NF-κB promotor activity in HEK293 cells stimulated or not with 4-OI prior to IKKβ wt or IKKβ C179A plasmid transfection. Data from one representative experiment in ( a ), two independent experiments in ( b ). Data are depicted as means ± SEM from two experiments in triplicates in ( c ), three independent experiments in ( d , e ). Data from one representative experiment out of three in ( f ). Data are depicted as means from one experiment in duplicates in ( h ). Data from one representative experiment performed twice in ( I , j ). Data are the means ± SEM from two experiments performed in quadruplicates in ( k ). Data are the means ± SEM from two experiments in triplicates in ( l ). Statistical significance by two-way ANOVA for ( c , l ) and one-way ANOVA for ( k ). Vertical stacks of bands are not derived from the same membrane in ( f , i , j ). Source data are provided in Source Data file.

    Techniques Used: Binding Assay, Confocal Microscopy, Translocation Assay, Enzyme-linked Immunosorbent Assay, Lysis, Liquid Chromatography with Mass Spectroscopy, Modification, Western Blot, Luciferase, Activity Assay, Plasmid Preparation, Transfection, Derivative Assay, Membrane

    kirc cell lines 786 o  (ATCC)


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  • 86

    Structured Review

    ATCC kirc cell lines 786 o
    Variant landscape of PCD genes in <t>KIRC</t> patients. ( A ) Heatmap and ( B ) Volcano plot showing differentially expressed PCD genes. Results of ( C ) Hallmark and ( D ) KEGG enrichment analyses for the differentially expressed genes. ( E ) An oncoplot of PCD-related genes in the TCGA cohort
    Kirc Cell Lines 786 O, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/kirc cell lines 786 o/product/ATCC
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    kirc cell lines 786 o - by Bioz Stars, 2024-05
    86/100 stars

    Images

    1) Product Images from "Assessing the role of programmed cell death signatures and related gene TOP2A in progression and prognostic prediction of clear cell renal cell carcinoma"

    Article Title: Assessing the role of programmed cell death signatures and related gene TOP2A in progression and prognostic prediction of clear cell renal cell carcinoma

    Journal: Cancer Cell International

    doi: 10.1186/s12935-024-03346-w

    Variant landscape of PCD genes in KIRC patients. ( A ) Heatmap and ( B ) Volcano plot showing differentially expressed PCD genes. Results of ( C ) Hallmark and ( D ) KEGG enrichment analyses for the differentially expressed genes. ( E ) An oncoplot of PCD-related genes in the TCGA cohort
    Figure Legend Snippet: Variant landscape of PCD genes in KIRC patients. ( A ) Heatmap and ( B ) Volcano plot showing differentially expressed PCD genes. Results of ( C ) Hallmark and ( D ) KEGG enrichment analyses for the differentially expressed genes. ( E ) An oncoplot of PCD-related genes in the TCGA cohort

    Techniques Used: Variant Assay

    Construction of a prognostic model for KIRC patients based on PCD genes. Univariate survival analysis of differentially expressed PCD genes in ( A ) TCGA, ( B ) E-MTAB-1980, ( C ) Braun-2020 cohorts. ( D ) Venn diagram showing the intersection among the three cohorts. ( E & F ) LASSO Cox regression to construct a prognostic model for KIRC patients. ( G - I ) Expression levels of PCDs, survival status, and seven genes in the three KIRC cohorts; (J-L) Impact of PCDs on OS of patients in the three KIRC cohorts
    Figure Legend Snippet: Construction of a prognostic model for KIRC patients based on PCD genes. Univariate survival analysis of differentially expressed PCD genes in ( A ) TCGA, ( B ) E-MTAB-1980, ( C ) Braun-2020 cohorts. ( D ) Venn diagram showing the intersection among the three cohorts. ( E & F ) LASSO Cox regression to construct a prognostic model for KIRC patients. ( G - I ) Expression levels of PCDs, survival status, and seven genes in the three KIRC cohorts; (J-L) Impact of PCDs on OS of patients in the three KIRC cohorts

    Techniques Used: Construct, Expressing

    Analysis of the clinical correlation of PCDs with KIRC patients.( A )The chromosomal location distribution of 7 genes. the expression correlation analysis of 7 genes in the ( B ) TCGA, ( C ) Braun-2020, and ( D ) E-MTAB-1980 cohorts. ( E ) Differences in PCDs values across different stages. ( F ) Differences in PCDs values across different T classifications. ( G ) Differences in PCDs values across different M classifications. ( H ) Differences in PCDs values across different N classifications; ( I ) Differences in PCDs values between recurrent and non-recurrent patients. ( J ) Differences in PCDs values between living and deceased patients. ( K ) Gene mutation analysis in the High-PCDs and Low-PCDs subgroups. ( L ) Correlation analysis of PCDs with the Hallmark signaling pathways. Correlation analysis of PCDs with the G2M checkpoint in the ( M ) TCGA, ( N ) Braun-2020, and ( O ) E-MTAB-1980 cohorts. *, p < 0.05; ***, p < 0.001
    Figure Legend Snippet: Analysis of the clinical correlation of PCDs with KIRC patients.( A )The chromosomal location distribution of 7 genes. the expression correlation analysis of 7 genes in the ( B ) TCGA, ( C ) Braun-2020, and ( D ) E-MTAB-1980 cohorts. ( E ) Differences in PCDs values across different stages. ( F ) Differences in PCDs values across different T classifications. ( G ) Differences in PCDs values across different M classifications. ( H ) Differences in PCDs values across different N classifications; ( I ) Differences in PCDs values between recurrent and non-recurrent patients. ( J ) Differences in PCDs values between living and deceased patients. ( K ) Gene mutation analysis in the High-PCDs and Low-PCDs subgroups. ( L ) Correlation analysis of PCDs with the Hallmark signaling pathways. Correlation analysis of PCDs with the G2M checkpoint in the ( M ) TCGA, ( N ) Braun-2020, and ( O ) E-MTAB-1980 cohorts. *, p < 0.05; ***, p < 0.001

    Techniques Used: Expressing, Mutagenesis

    Relationship between PCDs and the Immune Microenvironment. ( A ) Results of estimated scores and differential immune cell infiltration between High-PCDs and Low-PCDs subgroups in TCGA, assessed by CIBERSORT and ESTIMATE. In TCGA, the relative cell abundances of macrophages and Tregs between the two groups are calculated using ( B ) XCELL and ( C ) CIBERSORT. ( D ) Differentially expressed genes profile involved in the negative regulation of the Cancer-Immunity Cycle between High-PCDs and Low-PCDs subgroups. ( E ) Expression of common immune checkpoints between High-PCDs and Low-PCDs subgroups. ( F ) Expression of immunosuppressive cytokines between High-PCDs and Low-PCDs subgroups. ( G ) t-SNE plot visualization of all cell subtypes from KIRC patients in the GSE171306 cohort. ( H ) Bubble plot depicting the expression of model genes across different cell subtypes. ns, p > 0.05; *, p < 0.05; ***, p < 0.001
    Figure Legend Snippet: Relationship between PCDs and the Immune Microenvironment. ( A ) Results of estimated scores and differential immune cell infiltration between High-PCDs and Low-PCDs subgroups in TCGA, assessed by CIBERSORT and ESTIMATE. In TCGA, the relative cell abundances of macrophages and Tregs between the two groups are calculated using ( B ) XCELL and ( C ) CIBERSORT. ( D ) Differentially expressed genes profile involved in the negative regulation of the Cancer-Immunity Cycle between High-PCDs and Low-PCDs subgroups. ( E ) Expression of common immune checkpoints between High-PCDs and Low-PCDs subgroups. ( F ) Expression of immunosuppressive cytokines between High-PCDs and Low-PCDs subgroups. ( G ) t-SNE plot visualization of all cell subtypes from KIRC patients in the GSE171306 cohort. ( H ) Bubble plot depicting the expression of model genes across different cell subtypes. ns, p > 0.05; *, p < 0.05; ***, p < 0.001

    Techniques Used: Expressing

    Establishment and assessment of the nomogram survival model. ( A ) Univariate analysis for the clinicopathologic characteristics and PCDs in TCGA cohort. ( B ) Multivariate analysis for the clinicopathologic characteristics and PCDs in TCGA cohort. ( C ) A nomogram was established to predict the prognosis of Kidney Renal Clear Cell Carcinoma (KIRC) patients. ( D ) Calibration plots showing the probability of 1-, 3-, and 5-year overall survival in TCGA cohort. ( E ) Kaplan-Meier analyses for the two KIRC groups based on the nomogram score. ( G ) Receiver operator characteristic (ROC) analysis of the nomogram in TCGA cohort
    Figure Legend Snippet: Establishment and assessment of the nomogram survival model. ( A ) Univariate analysis for the clinicopathologic characteristics and PCDs in TCGA cohort. ( B ) Multivariate analysis for the clinicopathologic characteristics and PCDs in TCGA cohort. ( C ) A nomogram was established to predict the prognosis of Kidney Renal Clear Cell Carcinoma (KIRC) patients. ( D ) Calibration plots showing the probability of 1-, 3-, and 5-year overall survival in TCGA cohort. ( E ) Kaplan-Meier analyses for the two KIRC groups based on the nomogram score. ( G ) Receiver operator characteristic (ROC) analysis of the nomogram in TCGA cohort

    Techniques Used:

    TOP2A is overexpressed in KIRC and associated with poor prognosis. ( A ) Area under the curve (AUC) analysis of seven genes distinguishing KIRC tissue from adjacent non-cancerous tissue; Expression of TOP2A in KIRC tissue and adjacent non-cancerous tissue in ( B ) GSE14994, ( C ) GSE36895, ( D ) GSE40435, ( E ) GSE46699, ( F ) GSE53757, ( G ) GSE66272, ( H ) TCGA cohort. ( I ) Expression analysis of the TOP2A gene at different stages in the TCGA cohort. ( J ) Expression analysis of the TOP2A gene in different grades in the TCGA cohort. ( K ) Expression analysis of the TOP2A gene in different grades in the E-MTAB-1980 cohort. OS analysis of TOP2A in ( L ) TCGA, ( M ) Braun-2020, and ( N ) E-MTAB-1980 cohorts. ( O ) Disease-free survival (DFS) analysis of TOP2A in TCGA cohort. ***, p < 0.001
    Figure Legend Snippet: TOP2A is overexpressed in KIRC and associated with poor prognosis. ( A ) Area under the curve (AUC) analysis of seven genes distinguishing KIRC tissue from adjacent non-cancerous tissue; Expression of TOP2A in KIRC tissue and adjacent non-cancerous tissue in ( B ) GSE14994, ( C ) GSE36895, ( D ) GSE40435, ( E ) GSE46699, ( F ) GSE53757, ( G ) GSE66272, ( H ) TCGA cohort. ( I ) Expression analysis of the TOP2A gene at different stages in the TCGA cohort. ( J ) Expression analysis of the TOP2A gene in different grades in the TCGA cohort. ( K ) Expression analysis of the TOP2A gene in different grades in the E-MTAB-1980 cohort. OS analysis of TOP2A in ( L ) TCGA, ( M ) Braun-2020, and ( N ) E-MTAB-1980 cohorts. ( O ) Disease-free survival (DFS) analysis of TOP2A in TCGA cohort. ***, p < 0.001

    Techniques Used: Expressing

    TOP2A promotes proliferation and metastasis of KIRC cells. RT-PCR detection of TOP2A expression in ( A ) 786-O and ( B ) ACHN cells after knockdown of TOP2A. CCK8 assay to measure changes in proliferation ability after knockdown of TOP2A in ( C ) 786-O and ( D ) ACHN cells. Effect of TOP2A knockdown on ( E ) migration and ( G ) invasion ability of 786-O cells. Effect of TOP2A knockdown on ( F ) migration and ( H ) invasion ability of ACHN cells. Impact of TO P2A knockdown on ( I ) proliferation and ( J ) metastasis of ACHN cells in zebrafish. ns, p > 0.05; *, p < 0.05; **, p < 0.01; ***, p < 0.001
    Figure Legend Snippet: TOP2A promotes proliferation and metastasis of KIRC cells. RT-PCR detection of TOP2A expression in ( A ) 786-O and ( B ) ACHN cells after knockdown of TOP2A. CCK8 assay to measure changes in proliferation ability after knockdown of TOP2A in ( C ) 786-O and ( D ) ACHN cells. Effect of TOP2A knockdown on ( E ) migration and ( G ) invasion ability of 786-O cells. Effect of TOP2A knockdown on ( F ) migration and ( H ) invasion ability of ACHN cells. Impact of TO P2A knockdown on ( I ) proliferation and ( J ) metastasis of ACHN cells in zebrafish. ns, p > 0.05; *, p < 0.05; **, p < 0.01; ***, p < 0.001

    Techniques Used: Reverse Transcription Polymerase Chain Reaction, Expressing, CCK-8 Assay, Migration

    786 o  (ATCC)


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    ATCC 786 o
    CircPRELID2 expression is increased in RCC tissues and cells. A Cluster heat map of dysregulated circRNAs from 4 pairs of RCC tissues and adjacent normal tissues. B Schematic diagram of the biogenesis of circPRELID2 via back-splicing mechanism. CircPRELID2 expression by qRT-PCR in 52 pairs of clinical RCC tissues and matched healthy tissues ( C ), 29 cases RCC patients with TNM stage I + II and 23 cases patients with stage III ( D ), 30 cases RCC patients with negative lymph node metastasis and 22 cases patients with positive metastasis ( E ), HK2, A498, ACHN, RCC4, 769-P and <t>786-O</t> cells ( F ). * P < 0.05
    786 O, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "CircPRELID2 functions as a promoter of renal cell carcinoma through the miR-22-3p/ETV1 cascade"

    Article Title: CircPRELID2 functions as a promoter of renal cell carcinoma through the miR-22-3p/ETV1 cascade

    Journal: BMC Urology

    doi: 10.1186/s12894-024-01490-z

    CircPRELID2 expression is increased in RCC tissues and cells. A Cluster heat map of dysregulated circRNAs from 4 pairs of RCC tissues and adjacent normal tissues. B Schematic diagram of the biogenesis of circPRELID2 via back-splicing mechanism. CircPRELID2 expression by qRT-PCR in 52 pairs of clinical RCC tissues and matched healthy tissues ( C ), 29 cases RCC patients with TNM stage I + II and 23 cases patients with stage III ( D ), 30 cases RCC patients with negative lymph node metastasis and 22 cases patients with positive metastasis ( E ), HK2, A498, ACHN, RCC4, 769-P and 786-O cells ( F ). * P < 0.05
    Figure Legend Snippet: CircPRELID2 expression is increased in RCC tissues and cells. A Cluster heat map of dysregulated circRNAs from 4 pairs of RCC tissues and adjacent normal tissues. B Schematic diagram of the biogenesis of circPRELID2 via back-splicing mechanism. CircPRELID2 expression by qRT-PCR in 52 pairs of clinical RCC tissues and matched healthy tissues ( C ), 29 cases RCC patients with TNM stage I + II and 23 cases patients with stage III ( D ), 30 cases RCC patients with negative lymph node metastasis and 22 cases patients with positive metastasis ( E ), HK2, A498, ACHN, RCC4, 769-P and 786-O cells ( F ). * P < 0.05

    Techniques Used: Expressing, Quantitative RT-PCR

    CircPRELID2 is identified in RCC cells. A and B The expression levels of circPRELID2 by qRT-PCR in both RCC4 and 786-O cells treated with Actinomycin D for 4, 8, 12 and 24 h ( A ), in total RNA digested with RNase R for 15 min ( B ). C CircPRELID2 level by qRT-PCR in cytoplasm and nuclear fraction of RCC4 and 786-O cells, with U6 and 18S rRNA as internal controls. * P < 0.05
    Figure Legend Snippet: CircPRELID2 is identified in RCC cells. A and B The expression levels of circPRELID2 by qRT-PCR in both RCC4 and 786-O cells treated with Actinomycin D for 4, 8, 12 and 24 h ( A ), in total RNA digested with RNase R for 15 min ( B ). C CircPRELID2 level by qRT-PCR in cytoplasm and nuclear fraction of RCC4 and 786-O cells, with U6 and 18S rRNA as internal controls. * P < 0.05

    Techniques Used: Expressing, Quantitative RT-PCR

    CircPRELID2 silencing represses RCC cell malignant phenotypes in vitro and in vivo. A - I RCC4 and 786-O cells were transfected with sh-circPRELID2 or sh-NC, followed by the determination of circPRELID2 level by qRT-PCR after 48 h transfection ( A and B ), cell proliferation by CCK-8 assay after 24, 48 and 72 h transfection ( C and D ), cell colony formation using a standard colony formation assay ( E ), cell cycle progression by flow cytometry after 48 h transfection ( F and G ), cell migration and invasion by transwell assay after 24 h transfection ( H and I ). J - L sh-NC- or sh-circPRELID2-transduced RCC4 cells were injected into nude mice (5 mice each group). After 28 days, xenograft tumors were collected. J Growth curve of the xenografts. K Weight of the xenografts. L Immunohistochemistry for Ki-67 staining in the xenografts. * P < 0.05
    Figure Legend Snippet: CircPRELID2 silencing represses RCC cell malignant phenotypes in vitro and in vivo. A - I RCC4 and 786-O cells were transfected with sh-circPRELID2 or sh-NC, followed by the determination of circPRELID2 level by qRT-PCR after 48 h transfection ( A and B ), cell proliferation by CCK-8 assay after 24, 48 and 72 h transfection ( C and D ), cell colony formation using a standard colony formation assay ( E ), cell cycle progression by flow cytometry after 48 h transfection ( F and G ), cell migration and invasion by transwell assay after 24 h transfection ( H and I ). J - L sh-NC- or sh-circPRELID2-transduced RCC4 cells were injected into nude mice (5 mice each group). After 28 days, xenograft tumors were collected. J Growth curve of the xenografts. K Weight of the xenografts. L Immunohistochemistry for Ki-67 staining in the xenografts. * P < 0.05

    Techniques Used: In Vitro, In Vivo, Transfection, Quantitative RT-PCR, CCK-8 Assay, Colony Assay, Flow Cytometry, Migration, Transwell Assay, Injection, Immunohistochemistry, Staining

    CircPRELID2 acts as a miR-22-3p sponge to regulate ETV1 expression. A and B Cellular lysates of RCC4 and 786-O cells were incubated with anti-Ago2 or anti-IgG antibody, and then circPRELID2 level was detected by qRT-PCR. C Schematic model of the miR-22-3p-binding sites within circPRELID2 and the mutation in the seed sites. D Schematic of illuminating the miR-22-3p-binding sites within the 3’-UTR of ETV1 and mutated miR-22-3p-binding sites. E CircPRELID2 wide-type or mutant-type reporter construct (circPRELID2-WT or circPRELID2-MUT) was introduced into 293 T cells together with miR-22-3p mimic or miR-NC mimic, and then luciferase activity was assessed. F Relative luciferase activity in the cells co-transfected with ETV1 3’-UTR wild-type reporter (ETV1 3’-UTR-WT) or mutant-type reporter (ETV1 3’-UTR-MUT) and miR-NC mimic or miR-22-3p mimic. G MiR-22-3p expression was determined by qRT-PCR in RCC4 and 786-O cells transfected with sh-NC or sh-circPRELID2. H and I qRT-PCR and immunoblotting for ETV1 mRNA and protein levels in the cells transfected with miR-NC mimic or miR-22-3p mimic. J and K ETV1 expression in cells introduced with si-NC, si-circPRELID2, si-circPRELID2 + anti-miR-NC or si-circPRELID2 + anti-miR-22-3p. L MiR-22-3p expression was detected in 52 pairs of clinical RCC tissues and matched healthy tissues. (M and N) ETV1 expression in RCC tissues and matched healthy tissues. O - Q Expression correlations among miR-22-3p, circPRELID2, ETV1 were tested in RCC tissues using Spearman test. R MiR-22-3p expression was detected in HK2, RCC4 and 786-O cells. S ETV1 protein expression in HK2, RCC4 and 786-O cells. * P < 0.05
    Figure Legend Snippet: CircPRELID2 acts as a miR-22-3p sponge to regulate ETV1 expression. A and B Cellular lysates of RCC4 and 786-O cells were incubated with anti-Ago2 or anti-IgG antibody, and then circPRELID2 level was detected by qRT-PCR. C Schematic model of the miR-22-3p-binding sites within circPRELID2 and the mutation in the seed sites. D Schematic of illuminating the miR-22-3p-binding sites within the 3’-UTR of ETV1 and mutated miR-22-3p-binding sites. E CircPRELID2 wide-type or mutant-type reporter construct (circPRELID2-WT or circPRELID2-MUT) was introduced into 293 T cells together with miR-22-3p mimic or miR-NC mimic, and then luciferase activity was assessed. F Relative luciferase activity in the cells co-transfected with ETV1 3’-UTR wild-type reporter (ETV1 3’-UTR-WT) or mutant-type reporter (ETV1 3’-UTR-MUT) and miR-NC mimic or miR-22-3p mimic. G MiR-22-3p expression was determined by qRT-PCR in RCC4 and 786-O cells transfected with sh-NC or sh-circPRELID2. H and I qRT-PCR and immunoblotting for ETV1 mRNA and protein levels in the cells transfected with miR-NC mimic or miR-22-3p mimic. J and K ETV1 expression in cells introduced with si-NC, si-circPRELID2, si-circPRELID2 + anti-miR-NC or si-circPRELID2 + anti-miR-22-3p. L MiR-22-3p expression was detected in 52 pairs of clinical RCC tissues and matched healthy tissues. (M and N) ETV1 expression in RCC tissues and matched healthy tissues. O - Q Expression correlations among miR-22-3p, circPRELID2, ETV1 were tested in RCC tissues using Spearman test. R MiR-22-3p expression was detected in HK2, RCC4 and 786-O cells. S ETV1 protein expression in HK2, RCC4 and 786-O cells. * P < 0.05

    Techniques Used: Expressing, Incubation, Quantitative RT-PCR, Binding Assay, Mutagenesis, Construct, Luciferase, Activity Assay, Transfection, Western Blot

    CircPRELID2 silencing suppresses RCC cell malignant phenotypes by the miR-22-3p/ETV1 axis. A - H RCC4 and 786-O cells were transfected with sh-NC, sh-circPRELID2, sh-circPRELID2 + anti-miR-22-3p or sh-circPRELID2 + OE-ETV1. A Immunoblotting for ETV1 protein expression in the transfected cells. B and C Cell proliferation was assessed. D Cell colony formation using a standard colony formation assay. E and F Cell cycle progression by flow cytometry after 48 h transfection. G and H cell migration and invasion by transwell assay after 24 h transfection. I - L The culture media of transfected cells were collected and used to treat THP-1 monocytic leukemia cells co-treated with 100 ng/mL PMA (Sigma-Aldrich) for macrophage (THP1-M0) induction. After 24 h, the cells were assayed. I Flow cytometry for the CD206 + macrophages. J - L qRT-PCR for mRNA expression of Arg-1, IL-10 and TGF-β1. * P < 0.05
    Figure Legend Snippet: CircPRELID2 silencing suppresses RCC cell malignant phenotypes by the miR-22-3p/ETV1 axis. A - H RCC4 and 786-O cells were transfected with sh-NC, sh-circPRELID2, sh-circPRELID2 + anti-miR-22-3p or sh-circPRELID2 + OE-ETV1. A Immunoblotting for ETV1 protein expression in the transfected cells. B and C Cell proliferation was assessed. D Cell colony formation using a standard colony formation assay. E and F Cell cycle progression by flow cytometry after 48 h transfection. G and H cell migration and invasion by transwell assay after 24 h transfection. I - L The culture media of transfected cells were collected and used to treat THP-1 monocytic leukemia cells co-treated with 100 ng/mL PMA (Sigma-Aldrich) for macrophage (THP1-M0) induction. After 24 h, the cells were assayed. I Flow cytometry for the CD206 + macrophages. J - L qRT-PCR for mRNA expression of Arg-1, IL-10 and TGF-β1. * P < 0.05

    Techniques Used: Transfection, Western Blot, Expressing, Colony Assay, Flow Cytometry, Migration, Transwell Assay, Quantitative RT-PCR

    human ccrcc cell lines 786 o  (ATCC)


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    ATCC human ccrcc cell lines 786 o
    Human Ccrcc Cell Lines 786 O, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    human renal cell carcinoma 786 o  (ATCC)


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    ATCC human renal cell carcinoma 786 o
    Human Renal Cell Carcinoma 786 O, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    human renal cell carcinoma 786 o  (ATCC)


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    ATCC human renal cell carcinoma 786 o
    Human Renal Cell Carcinoma 786 O, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    786 o  (ATCC)


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    ATCC ccrcc cell lines 786 o
    Ccrcc Cell Lines 786 O, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    cell survival assay ccrcc cell lines 786 o  (ATCC)


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    ATCC cell survival assay ccrcc cell lines 786 o
    Cell Survival Assay Ccrcc Cell Lines 786 O, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    786 o  (ATCC)


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    ATCC 786 o
    CD70 Expression Analysis. A mRNA level of CD70 in TCGA sequencing database demonstrated various malignant tissue express higher CD70 compared with normal tissue, especially in KIRC and KIRP, two major types of RCC B CD70 mRNA level in RCC samples according to patient’s clinical stages showed significantly higher expression CD70 associated with later stages (Stage 3 and Stage 4) (n = 72 normal, n = 267 stage 1, n = 57 stage 2, n = 123 stage 3, n = 4 stage 4). C CD70 mRNA level in RCC samples according to pathological grading, showed higher CD70 expression related with higher grades (Grade 3 and Grade 4) (n = 72 normal, n = 14 grade 1, n = 229 grade 2, n = 206 grade 3, n = 76 grade 4). * P < 0.05, ** P < 0.01 *** P < 0.001, **** P < 0.0001 by unpaired Student t test. D Lower RCC patients survive related with higher CD70 expression (n = 185 low expression, n = 692 high expression) in TCGA database. E Representative immunohistochemical staining images for CD70 expression in samples from patients with KIRC, KIRP and KICH (Kidney Chromophobe). F Comparison of CD70 expression detected by IHC in samples from 109 RCC patients and 6 normal tissues. Total RCC patients and KIRC, KIRP but not KICH subtypes patients expressed significantly higher CD70 than the normal tissues. * P < 0.05, ** P < 0.01 by unpaired Student t test. G Cell surface CD70 expression in RCC cell lines detected by flow cytometry. All RCC cell lines <t>(786-O,</t> 769-P, A498, ACHN) expressed CD70 on cell surface. H Measurement of cell surface CD70 expression level in RCC cell line. Median fluorescence intensity (MFI) ratio calculated by the MFI detected with CD70 antibody divided by antibody isotypes control.
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    1) Product Images from "The development of chimeric antigen receptor T-cells against CD70 for renal cell carcinoma treatment"

    Article Title: The development of chimeric antigen receptor T-cells against CD70 for renal cell carcinoma treatment

    Journal: Journal of Translational Medicine

    doi: 10.1186/s12967-024-05101-1

    CD70 Expression Analysis. A mRNA level of CD70 in TCGA sequencing database demonstrated various malignant tissue express higher CD70 compared with normal tissue, especially in KIRC and KIRP, two major types of RCC B CD70 mRNA level in RCC samples according to patient’s clinical stages showed significantly higher expression CD70 associated with later stages (Stage 3 and Stage 4) (n = 72 normal, n = 267 stage 1, n = 57 stage 2, n = 123 stage 3, n = 4 stage 4). C CD70 mRNA level in RCC samples according to pathological grading, showed higher CD70 expression related with higher grades (Grade 3 and Grade 4) (n = 72 normal, n = 14 grade 1, n = 229 grade 2, n = 206 grade 3, n = 76 grade 4). * P < 0.05, ** P < 0.01 *** P < 0.001, **** P < 0.0001 by unpaired Student t test. D Lower RCC patients survive related with higher CD70 expression (n = 185 low expression, n = 692 high expression) in TCGA database. E Representative immunohistochemical staining images for CD70 expression in samples from patients with KIRC, KIRP and KICH (Kidney Chromophobe). F Comparison of CD70 expression detected by IHC in samples from 109 RCC patients and 6 normal tissues. Total RCC patients and KIRC, KIRP but not KICH subtypes patients expressed significantly higher CD70 than the normal tissues. * P < 0.05, ** P < 0.01 by unpaired Student t test. G Cell surface CD70 expression in RCC cell lines detected by flow cytometry. All RCC cell lines (786-O, 769-P, A498, ACHN) expressed CD70 on cell surface. H Measurement of cell surface CD70 expression level in RCC cell line. Median fluorescence intensity (MFI) ratio calculated by the MFI detected with CD70 antibody divided by antibody isotypes control.
    Figure Legend Snippet: CD70 Expression Analysis. A mRNA level of CD70 in TCGA sequencing database demonstrated various malignant tissue express higher CD70 compared with normal tissue, especially in KIRC and KIRP, two major types of RCC B CD70 mRNA level in RCC samples according to patient’s clinical stages showed significantly higher expression CD70 associated with later stages (Stage 3 and Stage 4) (n = 72 normal, n = 267 stage 1, n = 57 stage 2, n = 123 stage 3, n = 4 stage 4). C CD70 mRNA level in RCC samples according to pathological grading, showed higher CD70 expression related with higher grades (Grade 3 and Grade 4) (n = 72 normal, n = 14 grade 1, n = 229 grade 2, n = 206 grade 3, n = 76 grade 4). * P < 0.05, ** P < 0.01 *** P < 0.001, **** P < 0.0001 by unpaired Student t test. D Lower RCC patients survive related with higher CD70 expression (n = 185 low expression, n = 692 high expression) in TCGA database. E Representative immunohistochemical staining images for CD70 expression in samples from patients with KIRC, KIRP and KICH (Kidney Chromophobe). F Comparison of CD70 expression detected by IHC in samples from 109 RCC patients and 6 normal tissues. Total RCC patients and KIRC, KIRP but not KICH subtypes patients expressed significantly higher CD70 than the normal tissues. * P < 0.05, ** P < 0.01 by unpaired Student t test. G Cell surface CD70 expression in RCC cell lines detected by flow cytometry. All RCC cell lines (786-O, 769-P, A498, ACHN) expressed CD70 on cell surface. H Measurement of cell surface CD70 expression level in RCC cell line. Median fluorescence intensity (MFI) ratio calculated by the MFI detected with CD70 antibody divided by antibody isotypes control.

    Techniques Used: Expressing, Sequencing, Immunohistochemical staining, Staining, Comparison, Flow Cytometry, Fluorescence

    Generation and Characterization of CD70 CAR-T Cells A The amino acid sequences of CDR1-3 region of novel nanobody isolated from the phage library and identified as the specific binder to CD70. B CAR construct with CD8 α signal peptide (SP), scFv (41D12) or VHH (Nanobody), CD8 α hinge and transmembrane domain, intracellular 4-1BB co-stimulatory domain, and intracellular CD3 ζ activation domain. C CD70 CAR expression levels of 5 different donors measured by flow cytometry after transduction of activated T cells. CAR detected by biotin-labeled CD70 protein and BV421-conjugated streptavidin. D The percentage of CD70 CAR expressing T cells from 5 different health donors. All CAR highly expressed on T cell surface. E Antigen specific cytotoxicity of CAR-T cells. As CD70 positive cell lines (786-O, 769-P, ACHN, A498, K562 transduced with CD70) and CD70-negative cell lines (K562-WT, ACHN-CD70 KO) as a control, assessed by luciferase assay. All CAR-T cells were potent to kill CD70 positive target cell without cytotoxicity to antigen negative cells. F Antigen specific cytotoxicity of CD70 CAR-T cells against CD70-positive RCC cell lines (786-O, 769-P, ACHN, A498) during serial killing assays using luciferase assays. * P < 0.05, **** P < 0.0001 by two-way ANOVA with Dunnett's multiple comparisons test adjusted p value. G Fold change of CD3 + T cells in CD70 CAR-T co-culture with RCC cell lines during antigen stimulation in repetitive co-culture assay. H Analysis of cytokine production in the supernatants from repetitive co-cultures of RCC cells and CAR-T cells. The heatmap showed an increase in cytokines, including IL-2, TNF-α, IFN-γ, in the CD70 CAR-T cell groups
    Figure Legend Snippet: Generation and Characterization of CD70 CAR-T Cells A The amino acid sequences of CDR1-3 region of novel nanobody isolated from the phage library and identified as the specific binder to CD70. B CAR construct with CD8 α signal peptide (SP), scFv (41D12) or VHH (Nanobody), CD8 α hinge and transmembrane domain, intracellular 4-1BB co-stimulatory domain, and intracellular CD3 ζ activation domain. C CD70 CAR expression levels of 5 different donors measured by flow cytometry after transduction of activated T cells. CAR detected by biotin-labeled CD70 protein and BV421-conjugated streptavidin. D The percentage of CD70 CAR expressing T cells from 5 different health donors. All CAR highly expressed on T cell surface. E Antigen specific cytotoxicity of CAR-T cells. As CD70 positive cell lines (786-O, 769-P, ACHN, A498, K562 transduced with CD70) and CD70-negative cell lines (K562-WT, ACHN-CD70 KO) as a control, assessed by luciferase assay. All CAR-T cells were potent to kill CD70 positive target cell without cytotoxicity to antigen negative cells. F Antigen specific cytotoxicity of CD70 CAR-T cells against CD70-positive RCC cell lines (786-O, 769-P, ACHN, A498) during serial killing assays using luciferase assays. * P < 0.05, **** P < 0.0001 by two-way ANOVA with Dunnett's multiple comparisons test adjusted p value. G Fold change of CD3 + T cells in CD70 CAR-T co-culture with RCC cell lines during antigen stimulation in repetitive co-culture assay. H Analysis of cytokine production in the supernatants from repetitive co-cultures of RCC cells and CAR-T cells. The heatmap showed an increase in cytokines, including IL-2, TNF-α, IFN-γ, in the CD70 CAR-T cell groups

    Techniques Used: Isolation, Construct, Activation Assay, Expressing, Flow Cytometry, Transduction, Labeling, Luciferase, Co-Culture Assay, Co-culture Assay

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  • 86
    ATCC 786 o cells
    a Structures of itaconate, isomers and octyl-derivatives b <t>786-O</t> cells pretreated with octyl-derivatives (80 μM) or metabolites (25 mM) for 24 h, then infected with VSVΔ51 (MOI of 0.01). Virus-infected cells quantified by flow cytometry at 17 h post-infection. c Flow cytometry analysis of virus-infected cells in 786-O cells treated with increasing 4-OI concentrations at 17 h post-infection. d Host vs viral RNA ratio in VSVΔ51-infected 786-O cells (MOI of 0.01) with or without 4-OI (75 μM). e – g Cancer lines pretreated with 4-OI (125 μM or 75 μM for 786-O cells) for 24 h, then infected with VSVΔ51 at varying MOIs. Viral titers determined from supernatants 24 h post-infection. h 786-O cells pretreated with 4-OI (75 μM) for 24 h and infected with VSVΔ51 (MOI of 0.0001), followed by plaque imaging. Scale bars, 200 μm. i Plaque diameters measured 24 h after infection. j 786-O cellular layer integrity assessed by Calcein green staining after treatment with 4-OI (75 μM) and VSVΔ51 infection (MOI 0.01) for 24 h. Scale bars, 100 μm. k CT26WT cells treated with 4-OI (125 μM) for 24 h post-infection with VSVΔ51 (MOI 0.01) for 48 h. Cleaved caspase 3 in cyan blue, nuclei in dark blue stained with DAPI, and actin filaments with phalloidin in green. Scale bars, 100 μm. l , m CT26WT and 786-O cells pretreated with 4-OI (125 μM) and (75 μM), respectively, for 24 h, then infected with VSVΔ51 at a MOI of 0.01. Percentage of viable cells determined by flow cytometry at 30 h post-infection. Data are means ± SEM of two independent experiments in duplicates in ( b , c , e – g ) (except for CT26WT and 76-9, from one experiment in triplicates); one experiment in triplicates for ( d ); one experiment in multiple replicates for ( I ); and two experiments in triplicates for ( l , m ). Images are from one experiment in ( h ), one representative experiment out of two in ( j ), and one out of two in ( k ). Statistical significance indicated by one-way ANOVA for ( b , c , l , m ); and two-tailed Student’s t -test for ( e – g , i ). Source data provided in a Source Data file.
    786 O Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC kirc cell lines 786 o
    Variant landscape of PCD genes in <t>KIRC</t> patients. ( A ) Heatmap and ( B ) Volcano plot showing differentially expressed PCD genes. Results of ( C ) Hallmark and ( D ) KEGG enrichment analyses for the differentially expressed genes. ( E ) An oncoplot of PCD-related genes in the TCGA cohort
    Kirc Cell Lines 786 O, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    786 o  (ATCC)
    86
    ATCC 786 o
    CircPRELID2 expression is increased in RCC tissues and cells. A Cluster heat map of dysregulated circRNAs from 4 pairs of RCC tissues and adjacent normal tissues. B Schematic diagram of the biogenesis of circPRELID2 via back-splicing mechanism. CircPRELID2 expression by qRT-PCR in 52 pairs of clinical RCC tissues and matched healthy tissues ( C ), 29 cases RCC patients with TNM stage I + II and 23 cases patients with stage III ( D ), 30 cases RCC patients with negative lymph node metastasis and 22 cases patients with positive metastasis ( E ), HK2, A498, ACHN, RCC4, 769-P and <t>786-O</t> cells ( F ). * P < 0.05
    786 O, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC human ccrcc cell lines 786 o
    CircPRELID2 expression is increased in RCC tissues and cells. A Cluster heat map of dysregulated circRNAs from 4 pairs of RCC tissues and adjacent normal tissues. B Schematic diagram of the biogenesis of circPRELID2 via back-splicing mechanism. CircPRELID2 expression by qRT-PCR in 52 pairs of clinical RCC tissues and matched healthy tissues ( C ), 29 cases RCC patients with TNM stage I + II and 23 cases patients with stage III ( D ), 30 cases RCC patients with negative lymph node metastasis and 22 cases patients with positive metastasis ( E ), HK2, A498, ACHN, RCC4, 769-P and <t>786-O</t> cells ( F ). * P < 0.05
    Human Ccrcc Cell Lines 786 O, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC human renal cell carcinoma 786 o
    CircPRELID2 expression is increased in RCC tissues and cells. A Cluster heat map of dysregulated circRNAs from 4 pairs of RCC tissues and adjacent normal tissues. B Schematic diagram of the biogenesis of circPRELID2 via back-splicing mechanism. CircPRELID2 expression by qRT-PCR in 52 pairs of clinical RCC tissues and matched healthy tissues ( C ), 29 cases RCC patients with TNM stage I + II and 23 cases patients with stage III ( D ), 30 cases RCC patients with negative lymph node metastasis and 22 cases patients with positive metastasis ( E ), HK2, A498, ACHN, RCC4, 769-P and <t>786-O</t> cells ( F ). * P < 0.05
    Human Renal Cell Carcinoma 786 O, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    86
    ATCC ccrcc cell lines 786 o
    CircPRELID2 expression is increased in RCC tissues and cells. A Cluster heat map of dysregulated circRNAs from 4 pairs of RCC tissues and adjacent normal tissues. B Schematic diagram of the biogenesis of circPRELID2 via back-splicing mechanism. CircPRELID2 expression by qRT-PCR in 52 pairs of clinical RCC tissues and matched healthy tissues ( C ), 29 cases RCC patients with TNM stage I + II and 23 cases patients with stage III ( D ), 30 cases RCC patients with negative lymph node metastasis and 22 cases patients with positive metastasis ( E ), HK2, A498, ACHN, RCC4, 769-P and <t>786-O</t> cells ( F ). * P < 0.05
    Ccrcc Cell Lines 786 O, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC cell survival assay ccrcc cell lines 786 o
    CircPRELID2 expression is increased in RCC tissues and cells. A Cluster heat map of dysregulated circRNAs from 4 pairs of RCC tissues and adjacent normal tissues. B Schematic diagram of the biogenesis of circPRELID2 via back-splicing mechanism. CircPRELID2 expression by qRT-PCR in 52 pairs of clinical RCC tissues and matched healthy tissues ( C ), 29 cases RCC patients with TNM stage I + II and 23 cases patients with stage III ( D ), 30 cases RCC patients with negative lymph node metastasis and 22 cases patients with positive metastasis ( E ), HK2, A498, ACHN, RCC4, 769-P and <t>786-O</t> cells ( F ). * P < 0.05
    Cell Survival Assay Ccrcc Cell Lines 786 O, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    a Structures of itaconate, isomers and octyl-derivatives b 786-O cells pretreated with octyl-derivatives (80 μM) or metabolites (25 mM) for 24 h, then infected with VSVΔ51 (MOI of 0.01). Virus-infected cells quantified by flow cytometry at 17 h post-infection. c Flow cytometry analysis of virus-infected cells in 786-O cells treated with increasing 4-OI concentrations at 17 h post-infection. d Host vs viral RNA ratio in VSVΔ51-infected 786-O cells (MOI of 0.01) with or without 4-OI (75 μM). e – g Cancer lines pretreated with 4-OI (125 μM or 75 μM for 786-O cells) for 24 h, then infected with VSVΔ51 at varying MOIs. Viral titers determined from supernatants 24 h post-infection. h 786-O cells pretreated with 4-OI (75 μM) for 24 h and infected with VSVΔ51 (MOI of 0.0001), followed by plaque imaging. Scale bars, 200 μm. i Plaque diameters measured 24 h after infection. j 786-O cellular layer integrity assessed by Calcein green staining after treatment with 4-OI (75 μM) and VSVΔ51 infection (MOI 0.01) for 24 h. Scale bars, 100 μm. k CT26WT cells treated with 4-OI (125 μM) for 24 h post-infection with VSVΔ51 (MOI 0.01) for 48 h. Cleaved caspase 3 in cyan blue, nuclei in dark blue stained with DAPI, and actin filaments with phalloidin in green. Scale bars, 100 μm. l , m CT26WT and 786-O cells pretreated with 4-OI (125 μM) and (75 μM), respectively, for 24 h, then infected with VSVΔ51 at a MOI of 0.01. Percentage of viable cells determined by flow cytometry at 30 h post-infection. Data are means ± SEM of two independent experiments in duplicates in ( b , c , e – g ) (except for CT26WT and 76-9, from one experiment in triplicates); one experiment in triplicates for ( d ); one experiment in multiple replicates for ( I ); and two experiments in triplicates for ( l , m ). Images are from one experiment in ( h ), one representative experiment out of two in ( j ), and one out of two in ( k ). Statistical significance indicated by one-way ANOVA for ( b , c , l , m ); and two-tailed Student’s t -test for ( e – g , i ). Source data provided in a Source Data file.

    Journal: Nature Communications

    Article Title: Octyl itaconate enhances VSVΔ51 oncolytic virotherapy by multitarget inhibition of antiviral and inflammatory pathways

    doi: 10.1038/s41467-024-48422-x

    Figure Lengend Snippet: a Structures of itaconate, isomers and octyl-derivatives b 786-O cells pretreated with octyl-derivatives (80 μM) or metabolites (25 mM) for 24 h, then infected with VSVΔ51 (MOI of 0.01). Virus-infected cells quantified by flow cytometry at 17 h post-infection. c Flow cytometry analysis of virus-infected cells in 786-O cells treated with increasing 4-OI concentrations at 17 h post-infection. d Host vs viral RNA ratio in VSVΔ51-infected 786-O cells (MOI of 0.01) with or without 4-OI (75 μM). e – g Cancer lines pretreated with 4-OI (125 μM or 75 μM for 786-O cells) for 24 h, then infected with VSVΔ51 at varying MOIs. Viral titers determined from supernatants 24 h post-infection. h 786-O cells pretreated with 4-OI (75 μM) for 24 h and infected with VSVΔ51 (MOI of 0.0001), followed by plaque imaging. Scale bars, 200 μm. i Plaque diameters measured 24 h after infection. j 786-O cellular layer integrity assessed by Calcein green staining after treatment with 4-OI (75 μM) and VSVΔ51 infection (MOI 0.01) for 24 h. Scale bars, 100 μm. k CT26WT cells treated with 4-OI (125 μM) for 24 h post-infection with VSVΔ51 (MOI 0.01) for 48 h. Cleaved caspase 3 in cyan blue, nuclei in dark blue stained with DAPI, and actin filaments with phalloidin in green. Scale bars, 100 μm. l , m CT26WT and 786-O cells pretreated with 4-OI (125 μM) and (75 μM), respectively, for 24 h, then infected with VSVΔ51 at a MOI of 0.01. Percentage of viable cells determined by flow cytometry at 30 h post-infection. Data are means ± SEM of two independent experiments in duplicates in ( b , c , e – g ) (except for CT26WT and 76-9, from one experiment in triplicates); one experiment in triplicates for ( d ); one experiment in multiple replicates for ( I ); and two experiments in triplicates for ( l , m ). Images are from one experiment in ( h ), one representative experiment out of two in ( j ), and one out of two in ( k ). Statistical significance indicated by one-way ANOVA for ( b , c , l , m ); and two-tailed Student’s t -test for ( e – g , i ). Source data provided in a Source Data file.

    Article Snippet: 786-O cells were purchased from ATCC.

    Techniques: Infection, Virus, Flow Cytometry, Imaging, Staining, Two Tailed Test

    a NRF2 protein levels in control and NRF2 knockout (KO) 786-O cells treated with 4-OI (75 μM) for 24 h using confocal microscopy. Blue: actin filaments, green: NRF2. Scale bars, 50 μm. b KEAP1 levels analyzed in 786-O cells treated with alkynated 4-OI (4-OI-alk) (125 μM) for 4 or 24 h with or without non-alkynated 4-OI (125 μM) by anti-KEAP1 immunoblotting. c Viral RNA content assessed by RNA sequencing in VSVΔ51-infected (MOI of 0.01) control and NRF2 KO 786-O cells with or without 4-OI (75 μM) pretreatment. d – f Immunoblot analysis in control and NRF2 KO cells pretreated with 4-OI (75 μM) before VSVΔ51 challenge (MOI of 0.01) ( d ). Fluorescence microscopy showing VSVΔ51-RFP spread and cellular layer integrity with Hoechst stain overlay (Scale bars, 300 μm) ( e ) and quantification of infected cells by flow cytometry at 17 h post-infection ( f ). g – j Quantification of virus-infected cells by flow cytometry in 786-O cells transiently KO for NRF2 ( g ) or KEAP1 ( j ). Immunoblot analysis in NRF2 KO ( h ) and KEAP1 KO cells ( i ) pretreated with 4-OI (75 μM) before VSVΔ51 challenge (MOI of 0.01). k 786-O cells incubated with L-NAC (1 mM) for 3 h before 4-OI challenge (75 μM) for 24 h, then infected with VSVΔ51-RFP (MOI of 0.01). Quantification of infected cells by flow cytometry at 17 h post-infection. Data are means ± SEM from two independent experiments in biological duplicates and triplicates in ( f ), and in biological triplicates and quadruplicates in ( g ). Two experiments in biological quadruplicates in ( j ) and ( k ). Images from one representative experiment in triplicates in ( a ) and ( e ). Data in ( b ) and ( d ) from one representative of three independent experiments. Data as means ± SEM from one experiment in biological triplicates in ( c ). Statistics indicate significance by one-way ANOVA for ( f , g , j , k ). Vertical stacks of bands are not derived from the same membrane in ( d , h , I ). Source data provided in the Source Data file.

    Journal: Nature Communications

    Article Title: Octyl itaconate enhances VSVΔ51 oncolytic virotherapy by multitarget inhibition of antiviral and inflammatory pathways

    doi: 10.1038/s41467-024-48422-x

    Figure Lengend Snippet: a NRF2 protein levels in control and NRF2 knockout (KO) 786-O cells treated with 4-OI (75 μM) for 24 h using confocal microscopy. Blue: actin filaments, green: NRF2. Scale bars, 50 μm. b KEAP1 levels analyzed in 786-O cells treated with alkynated 4-OI (4-OI-alk) (125 μM) for 4 or 24 h with or without non-alkynated 4-OI (125 μM) by anti-KEAP1 immunoblotting. c Viral RNA content assessed by RNA sequencing in VSVΔ51-infected (MOI of 0.01) control and NRF2 KO 786-O cells with or without 4-OI (75 μM) pretreatment. d – f Immunoblot analysis in control and NRF2 KO cells pretreated with 4-OI (75 μM) before VSVΔ51 challenge (MOI of 0.01) ( d ). Fluorescence microscopy showing VSVΔ51-RFP spread and cellular layer integrity with Hoechst stain overlay (Scale bars, 300 μm) ( e ) and quantification of infected cells by flow cytometry at 17 h post-infection ( f ). g – j Quantification of virus-infected cells by flow cytometry in 786-O cells transiently KO for NRF2 ( g ) or KEAP1 ( j ). Immunoblot analysis in NRF2 KO ( h ) and KEAP1 KO cells ( i ) pretreated with 4-OI (75 μM) before VSVΔ51 challenge (MOI of 0.01). k 786-O cells incubated with L-NAC (1 mM) for 3 h before 4-OI challenge (75 μM) for 24 h, then infected with VSVΔ51-RFP (MOI of 0.01). Quantification of infected cells by flow cytometry at 17 h post-infection. Data are means ± SEM from two independent experiments in biological duplicates and triplicates in ( f ), and in biological triplicates and quadruplicates in ( g ). Two experiments in biological quadruplicates in ( j ) and ( k ). Images from one representative experiment in triplicates in ( a ) and ( e ). Data in ( b ) and ( d ) from one representative of three independent experiments. Data as means ± SEM from one experiment in biological triplicates in ( c ). Statistics indicate significance by one-way ANOVA for ( f , g , j , k ). Vertical stacks of bands are not derived from the same membrane in ( d , h , I ). Source data provided in the Source Data file.

    Article Snippet: 786-O cells were purchased from ATCC.

    Techniques: Knock-Out, Confocal Microscopy, Western Blot, RNA Sequencing Assay, Infection, Fluorescence, Microscopy, Staining, Flow Cytometry, Virus, Incubation, Derivative Assay, Membrane

    a – c 786-O cells pretreated with 4-OI (75 μM) for 24 h and infected with VSVΔ51 (MOI 0.01) for 17 h. RNA sequencing analysis emphasizing on antiviral genes (blue dots) in the volcano plot ( a ), differentially expressed interferon-stimulated genes (ISGs) in the heat map ( b ), and top KEGG pathways affected by 4-OI during viral infection (one-sided hypergeometric test, Benjamini–Hochberg method was applied to adjust the p -value for multiple testing) ( c ). d , e 786-O cells pretreated with 4-OI (125 μM) for 24 h and infected with VSVΔ51-RFP (MOI 0.01) for 24 h. IFIT1 levels assessed by fluorescence microscopy ( d ), and Western blot performed on cell lysates for antiviral proteins ( e ). f 786-O cells pretreated with 4-OI (75 μM) for 24 h infected with wild-type VSV (wt VSV) or VSVΔ51 at MOI 0.01. Viral titers determined 24 h post-infection. g – i Control and NRF2 KO 786-O cells, as well as 786-O cells transiently KO for NRF2 or KEAP using CRISPR/Cas9, pretreated with 4-OI (75 μM) for 24 h and infected with VSVΔ51 (MOI 0.01) for 17 h. Immunoblots in ( g , h ). CXCL10 release measured by ELISA from supernatants in ( I ). j Control and NRF2 KO 786-O cells pretreated with 4-OI (75 μM) for 24 h and stimulated with the RIG-I agonist M8 (3.5 ng/mL) for 5 h. Western blot performed on cell lysates. Data are from one experiment performed in triplicate in ( a – c ). Images are from one experiment in ( d ). Data are from one representative experiment performed at least three times in ( e ). Data are depicted as means ± SEM from one experiment performed in triplicate in ( f ). Data are from one representative experiment out of three in ( g ), out of two in ( h ) and ( j ). Data are depicted as means ± SEM from two experiments performed in triplicate in ( I ). Statistics indicate significance by two-way ANOVA for ( f , I ). Vertical stacks of bands are not derived from the same membrane in ( e , g , h , j ). Source data provided as a Source Data file.

    Journal: Nature Communications

    Article Title: Octyl itaconate enhances VSVΔ51 oncolytic virotherapy by multitarget inhibition of antiviral and inflammatory pathways

    doi: 10.1038/s41467-024-48422-x

    Figure Lengend Snippet: a – c 786-O cells pretreated with 4-OI (75 μM) for 24 h and infected with VSVΔ51 (MOI 0.01) for 17 h. RNA sequencing analysis emphasizing on antiviral genes (blue dots) in the volcano plot ( a ), differentially expressed interferon-stimulated genes (ISGs) in the heat map ( b ), and top KEGG pathways affected by 4-OI during viral infection (one-sided hypergeometric test, Benjamini–Hochberg method was applied to adjust the p -value for multiple testing) ( c ). d , e 786-O cells pretreated with 4-OI (125 μM) for 24 h and infected with VSVΔ51-RFP (MOI 0.01) for 24 h. IFIT1 levels assessed by fluorescence microscopy ( d ), and Western blot performed on cell lysates for antiviral proteins ( e ). f 786-O cells pretreated with 4-OI (75 μM) for 24 h infected with wild-type VSV (wt VSV) or VSVΔ51 at MOI 0.01. Viral titers determined 24 h post-infection. g – i Control and NRF2 KO 786-O cells, as well as 786-O cells transiently KO for NRF2 or KEAP using CRISPR/Cas9, pretreated with 4-OI (75 μM) for 24 h and infected with VSVΔ51 (MOI 0.01) for 17 h. Immunoblots in ( g , h ). CXCL10 release measured by ELISA from supernatants in ( I ). j Control and NRF2 KO 786-O cells pretreated with 4-OI (75 μM) for 24 h and stimulated with the RIG-I agonist M8 (3.5 ng/mL) for 5 h. Western blot performed on cell lysates. Data are from one experiment performed in triplicate in ( a – c ). Images are from one experiment in ( d ). Data are from one representative experiment performed at least three times in ( e ). Data are depicted as means ± SEM from one experiment performed in triplicate in ( f ). Data are from one representative experiment out of three in ( g ), out of two in ( h ) and ( j ). Data are depicted as means ± SEM from two experiments performed in triplicate in ( I ). Statistics indicate significance by two-way ANOVA for ( f , I ). Vertical stacks of bands are not derived from the same membrane in ( e , g , h , j ). Source data provided as a Source Data file.

    Article Snippet: 786-O cells were purchased from ATCC.

    Techniques: Infection, RNA Sequencing Assay, Fluorescence, Microscopy, Western Blot, CRISPR, Enzyme-linked Immunosorbent Assay, Derivative Assay, Membrane

    a HEK293 cells pretreated with increasing 4-OI concentrations (75 and 125 μM) and transfected with GFP-tagged plasmids. Immunoblotting analyzes antiviral proteins. b , c Data from Runtsch et al. . THP1 cells treated with 4-OI (125 μM), prior challenge with IA-DTB, cell lysis, and measurement of modified cysteines by LC-MS. d 786-O cells treated with 125 μM of 4-OI-alk (4 or 24 h) with or without 4-OI (125 μM), followed by click chemistry and biotin enrichment. Samples before and after enrichment analyzed by anti-MAVS immunoblotting. e HEK293 cells pretreated or not with 4-OI (125 μM) and transfected with Flag-tagged MAVS together with GFP-tagged RIG-I or TBK1 as indicated. Whole-cell extracts prepared and immunoprecipitated with anti-Flag antibody M2; immunoprecipitated complexes or 5% input run on SDS-PAGE and probed with anti-GFP/anti-Flag antibodies. f , g Transient MAVS KO 786-O cells treated with 4-OI, then infected with VSVΔ51, analyzed by Western blot ( f ) and flow cytometry ( g ). h HEK293 cells transfected with a plasmid encoding Flag-tagged MAVS wt or mutant Flag-tagged MAVS C283A for 24 h. Subsequently, cells treated with 125 μM of alkynated 4-OI (4-OI-alk) for 4 h, followed by click chemistry and biotin enrichment. Samples before and after enrichment analyzed by anti-Flag immunoblotting. i HEK293 cells stimulated with 4-OI prior to transfection with MAVS wt or mutant C283A MAVS, analyzed by ISRE promoter luciferase activity. j HEK293 cells transfected with MAVS wt or mutant together with TBK1, treated with 4-OI, analyzed by immunoprecipitation and immunoblotting. Data from one representative experiment in ( a ), three independent experiments in ( b , c ), one representative experiment performed three times in ( d ), one experiment in ( e , h , j ). Data from one representative experiment out of two in ( f ). Data depicted as means ± SEM from two independent experiments performed in triplicates and quadruplicates in ( g ), two independent experiments in triplicates in ( I ). Statistical significance by one-way ANOVA for ( g ) and two-way ANOVA for ( I ). Vertical stacks of bands are not derived from the same membrane in ( a , e , f , j ). Source data provided in Source Data file.

    Journal: Nature Communications

    Article Title: Octyl itaconate enhances VSVΔ51 oncolytic virotherapy by multitarget inhibition of antiviral and inflammatory pathways

    doi: 10.1038/s41467-024-48422-x

    Figure Lengend Snippet: a HEK293 cells pretreated with increasing 4-OI concentrations (75 and 125 μM) and transfected with GFP-tagged plasmids. Immunoblotting analyzes antiviral proteins. b , c Data from Runtsch et al. . THP1 cells treated with 4-OI (125 μM), prior challenge with IA-DTB, cell lysis, and measurement of modified cysteines by LC-MS. d 786-O cells treated with 125 μM of 4-OI-alk (4 or 24 h) with or without 4-OI (125 μM), followed by click chemistry and biotin enrichment. Samples before and after enrichment analyzed by anti-MAVS immunoblotting. e HEK293 cells pretreated or not with 4-OI (125 μM) and transfected with Flag-tagged MAVS together with GFP-tagged RIG-I or TBK1 as indicated. Whole-cell extracts prepared and immunoprecipitated with anti-Flag antibody M2; immunoprecipitated complexes or 5% input run on SDS-PAGE and probed with anti-GFP/anti-Flag antibodies. f , g Transient MAVS KO 786-O cells treated with 4-OI, then infected with VSVΔ51, analyzed by Western blot ( f ) and flow cytometry ( g ). h HEK293 cells transfected with a plasmid encoding Flag-tagged MAVS wt or mutant Flag-tagged MAVS C283A for 24 h. Subsequently, cells treated with 125 μM of alkynated 4-OI (4-OI-alk) for 4 h, followed by click chemistry and biotin enrichment. Samples before and after enrichment analyzed by anti-Flag immunoblotting. i HEK293 cells stimulated with 4-OI prior to transfection with MAVS wt or mutant C283A MAVS, analyzed by ISRE promoter luciferase activity. j HEK293 cells transfected with MAVS wt or mutant together with TBK1, treated with 4-OI, analyzed by immunoprecipitation and immunoblotting. Data from one representative experiment in ( a ), three independent experiments in ( b , c ), one representative experiment performed three times in ( d ), one experiment in ( e , h , j ). Data from one representative experiment out of two in ( f ). Data depicted as means ± SEM from two independent experiments performed in triplicates and quadruplicates in ( g ), two independent experiments in triplicates in ( I ). Statistical significance by one-way ANOVA for ( g ) and two-way ANOVA for ( I ). Vertical stacks of bands are not derived from the same membrane in ( a , e , f , j ). Source data provided in Source Data file.

    Article Snippet: 786-O cells were purchased from ATCC.

    Techniques: Transfection, Western Blot, Lysis, Modification, Liquid Chromatography with Mass Spectroscopy, Immunoprecipitation, SDS Page, Infection, Flow Cytometry, Plasmid Preparation, Mutagenesis, Luciferase, Activity Assay, Derivative Assay, Membrane

    a CiiiDER analysis to identify overrepresented transcription factor binding sites in 786-O cells treated or not with 4-OI (75 µM) prior VSVΔ51 (MOI 0.01 for 17 h). b , c Confocal microscopy of p65 nuclear translocation in 786-O cells treated or not with 4-OI following VSVΔ51 (Scale, 20 μm) ( b ); IL-6 levels measured by ELISA ( c ). d , e Data from Runtsch et al. . THP1 cells treated with 4-OI following IA-DTB, cell lysis, and LC-MS measurements of modified cysteines. f 786-O cells upon 4-OI-alk with or without 4-OI (both 125 µM). Immunoblotting of IKKβ, IKKγ, and IKK ε before and after biotin enrichment. g Illustration of 4-OI binding (green) to IKKβ at Cys179 (left) and 2D ligand-protein interactions (right). Lipophilicity protein surface: lipophilic (cyan), hydrophilic (violet), neutral (white), α-helices (cyan), β-sheets (yellow), loops (cyan). h Luciferase NF-kB promotor activity in control and NRF2 KO 786-O treated or not with 4-OI prior to control (pc) or IKKβ plasmid transfection. i Immunoblotting of IKKα/β, IκBα, and P65 phosphorylation in 786-O cells treated or not with 4-OI prior VSVΔ51. j , k IKKβ KO 786-O cells treated or not with 4-OI following VSVΔ51, immunoblotting ( j ) and flow ( k ) analyses. l Luciferase assay of NF-κB promotor activity in HEK293 cells stimulated or not with 4-OI prior to IKKβ wt or IKKβ C179A plasmid transfection. Data from one representative experiment in ( a ), two independent experiments in ( b ). Data are depicted as means ± SEM from two experiments in triplicates in ( c ), three independent experiments in ( d , e ). Data from one representative experiment out of three in ( f ). Data are depicted as means from one experiment in duplicates in ( h ). Data from one representative experiment performed twice in ( I , j ). Data are the means ± SEM from two experiments performed in quadruplicates in ( k ). Data are the means ± SEM from two experiments in triplicates in ( l ). Statistical significance by two-way ANOVA for ( c , l ) and one-way ANOVA for ( k ). Vertical stacks of bands are not derived from the same membrane in ( f , i , j ). Source data are provided in Source Data file.

    Journal: Nature Communications

    Article Title: Octyl itaconate enhances VSVΔ51 oncolytic virotherapy by multitarget inhibition of antiviral and inflammatory pathways

    doi: 10.1038/s41467-024-48422-x

    Figure Lengend Snippet: a CiiiDER analysis to identify overrepresented transcription factor binding sites in 786-O cells treated or not with 4-OI (75 µM) prior VSVΔ51 (MOI 0.01 for 17 h). b , c Confocal microscopy of p65 nuclear translocation in 786-O cells treated or not with 4-OI following VSVΔ51 (Scale, 20 μm) ( b ); IL-6 levels measured by ELISA ( c ). d , e Data from Runtsch et al. . THP1 cells treated with 4-OI following IA-DTB, cell lysis, and LC-MS measurements of modified cysteines. f 786-O cells upon 4-OI-alk with or without 4-OI (both 125 µM). Immunoblotting of IKKβ, IKKγ, and IKK ε before and after biotin enrichment. g Illustration of 4-OI binding (green) to IKKβ at Cys179 (left) and 2D ligand-protein interactions (right). Lipophilicity protein surface: lipophilic (cyan), hydrophilic (violet), neutral (white), α-helices (cyan), β-sheets (yellow), loops (cyan). h Luciferase NF-kB promotor activity in control and NRF2 KO 786-O treated or not with 4-OI prior to control (pc) or IKKβ plasmid transfection. i Immunoblotting of IKKα/β, IκBα, and P65 phosphorylation in 786-O cells treated or not with 4-OI prior VSVΔ51. j , k IKKβ KO 786-O cells treated or not with 4-OI following VSVΔ51, immunoblotting ( j ) and flow ( k ) analyses. l Luciferase assay of NF-κB promotor activity in HEK293 cells stimulated or not with 4-OI prior to IKKβ wt or IKKβ C179A plasmid transfection. Data from one representative experiment in ( a ), two independent experiments in ( b ). Data are depicted as means ± SEM from two experiments in triplicates in ( c ), three independent experiments in ( d , e ). Data from one representative experiment out of three in ( f ). Data are depicted as means from one experiment in duplicates in ( h ). Data from one representative experiment performed twice in ( I , j ). Data are the means ± SEM from two experiments performed in quadruplicates in ( k ). Data are the means ± SEM from two experiments in triplicates in ( l ). Statistical significance by two-way ANOVA for ( c , l ) and one-way ANOVA for ( k ). Vertical stacks of bands are not derived from the same membrane in ( f , i , j ). Source data are provided in Source Data file.

    Article Snippet: 786-O cells were purchased from ATCC.

    Techniques: Binding Assay, Confocal Microscopy, Translocation Assay, Enzyme-linked Immunosorbent Assay, Lysis, Liquid Chromatography with Mass Spectroscopy, Modification, Western Blot, Luciferase, Activity Assay, Plasmid Preparation, Transfection, Derivative Assay, Membrane

    Variant landscape of PCD genes in KIRC patients. ( A ) Heatmap and ( B ) Volcano plot showing differentially expressed PCD genes. Results of ( C ) Hallmark and ( D ) KEGG enrichment analyses for the differentially expressed genes. ( E ) An oncoplot of PCD-related genes in the TCGA cohort

    Journal: Cancer Cell International

    Article Title: Assessing the role of programmed cell death signatures and related gene TOP2A in progression and prognostic prediction of clear cell renal cell carcinoma

    doi: 10.1186/s12935-024-03346-w

    Figure Lengend Snippet: Variant landscape of PCD genes in KIRC patients. ( A ) Heatmap and ( B ) Volcano plot showing differentially expressed PCD genes. Results of ( C ) Hallmark and ( D ) KEGG enrichment analyses for the differentially expressed genes. ( E ) An oncoplot of PCD-related genes in the TCGA cohort

    Article Snippet: The KIRC cell lines 786-O and ACHN were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: Variant Assay

    Construction of a prognostic model for KIRC patients based on PCD genes. Univariate survival analysis of differentially expressed PCD genes in ( A ) TCGA, ( B ) E-MTAB-1980, ( C ) Braun-2020 cohorts. ( D ) Venn diagram showing the intersection among the three cohorts. ( E & F ) LASSO Cox regression to construct a prognostic model for KIRC patients. ( G - I ) Expression levels of PCDs, survival status, and seven genes in the three KIRC cohorts; (J-L) Impact of PCDs on OS of patients in the three KIRC cohorts

    Journal: Cancer Cell International

    Article Title: Assessing the role of programmed cell death signatures and related gene TOP2A in progression and prognostic prediction of clear cell renal cell carcinoma

    doi: 10.1186/s12935-024-03346-w

    Figure Lengend Snippet: Construction of a prognostic model for KIRC patients based on PCD genes. Univariate survival analysis of differentially expressed PCD genes in ( A ) TCGA, ( B ) E-MTAB-1980, ( C ) Braun-2020 cohorts. ( D ) Venn diagram showing the intersection among the three cohorts. ( E & F ) LASSO Cox regression to construct a prognostic model for KIRC patients. ( G - I ) Expression levels of PCDs, survival status, and seven genes in the three KIRC cohorts; (J-L) Impact of PCDs on OS of patients in the three KIRC cohorts

    Article Snippet: The KIRC cell lines 786-O and ACHN were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: Construct, Expressing

    Analysis of the clinical correlation of PCDs with KIRC patients.( A )The chromosomal location distribution of 7 genes. the expression correlation analysis of 7 genes in the ( B ) TCGA, ( C ) Braun-2020, and ( D ) E-MTAB-1980 cohorts. ( E ) Differences in PCDs values across different stages. ( F ) Differences in PCDs values across different T classifications. ( G ) Differences in PCDs values across different M classifications. ( H ) Differences in PCDs values across different N classifications; ( I ) Differences in PCDs values between recurrent and non-recurrent patients. ( J ) Differences in PCDs values between living and deceased patients. ( K ) Gene mutation analysis in the High-PCDs and Low-PCDs subgroups. ( L ) Correlation analysis of PCDs with the Hallmark signaling pathways. Correlation analysis of PCDs with the G2M checkpoint in the ( M ) TCGA, ( N ) Braun-2020, and ( O ) E-MTAB-1980 cohorts. *, p < 0.05; ***, p < 0.001

    Journal: Cancer Cell International

    Article Title: Assessing the role of programmed cell death signatures and related gene TOP2A in progression and prognostic prediction of clear cell renal cell carcinoma

    doi: 10.1186/s12935-024-03346-w

    Figure Lengend Snippet: Analysis of the clinical correlation of PCDs with KIRC patients.( A )The chromosomal location distribution of 7 genes. the expression correlation analysis of 7 genes in the ( B ) TCGA, ( C ) Braun-2020, and ( D ) E-MTAB-1980 cohorts. ( E ) Differences in PCDs values across different stages. ( F ) Differences in PCDs values across different T classifications. ( G ) Differences in PCDs values across different M classifications. ( H ) Differences in PCDs values across different N classifications; ( I ) Differences in PCDs values between recurrent and non-recurrent patients. ( J ) Differences in PCDs values between living and deceased patients. ( K ) Gene mutation analysis in the High-PCDs and Low-PCDs subgroups. ( L ) Correlation analysis of PCDs with the Hallmark signaling pathways. Correlation analysis of PCDs with the G2M checkpoint in the ( M ) TCGA, ( N ) Braun-2020, and ( O ) E-MTAB-1980 cohorts. *, p < 0.05; ***, p < 0.001

    Article Snippet: The KIRC cell lines 786-O and ACHN were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: Expressing, Mutagenesis

    Relationship between PCDs and the Immune Microenvironment. ( A ) Results of estimated scores and differential immune cell infiltration between High-PCDs and Low-PCDs subgroups in TCGA, assessed by CIBERSORT and ESTIMATE. In TCGA, the relative cell abundances of macrophages and Tregs between the two groups are calculated using ( B ) XCELL and ( C ) CIBERSORT. ( D ) Differentially expressed genes profile involved in the negative regulation of the Cancer-Immunity Cycle between High-PCDs and Low-PCDs subgroups. ( E ) Expression of common immune checkpoints between High-PCDs and Low-PCDs subgroups. ( F ) Expression of immunosuppressive cytokines between High-PCDs and Low-PCDs subgroups. ( G ) t-SNE plot visualization of all cell subtypes from KIRC patients in the GSE171306 cohort. ( H ) Bubble plot depicting the expression of model genes across different cell subtypes. ns, p > 0.05; *, p < 0.05; ***, p < 0.001

    Journal: Cancer Cell International

    Article Title: Assessing the role of programmed cell death signatures and related gene TOP2A in progression and prognostic prediction of clear cell renal cell carcinoma

    doi: 10.1186/s12935-024-03346-w

    Figure Lengend Snippet: Relationship between PCDs and the Immune Microenvironment. ( A ) Results of estimated scores and differential immune cell infiltration between High-PCDs and Low-PCDs subgroups in TCGA, assessed by CIBERSORT and ESTIMATE. In TCGA, the relative cell abundances of macrophages and Tregs between the two groups are calculated using ( B ) XCELL and ( C ) CIBERSORT. ( D ) Differentially expressed genes profile involved in the negative regulation of the Cancer-Immunity Cycle between High-PCDs and Low-PCDs subgroups. ( E ) Expression of common immune checkpoints between High-PCDs and Low-PCDs subgroups. ( F ) Expression of immunosuppressive cytokines between High-PCDs and Low-PCDs subgroups. ( G ) t-SNE plot visualization of all cell subtypes from KIRC patients in the GSE171306 cohort. ( H ) Bubble plot depicting the expression of model genes across different cell subtypes. ns, p > 0.05; *, p < 0.05; ***, p < 0.001

    Article Snippet: The KIRC cell lines 786-O and ACHN were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: Expressing

    Establishment and assessment of the nomogram survival model. ( A ) Univariate analysis for the clinicopathologic characteristics and PCDs in TCGA cohort. ( B ) Multivariate analysis for the clinicopathologic characteristics and PCDs in TCGA cohort. ( C ) A nomogram was established to predict the prognosis of Kidney Renal Clear Cell Carcinoma (KIRC) patients. ( D ) Calibration plots showing the probability of 1-, 3-, and 5-year overall survival in TCGA cohort. ( E ) Kaplan-Meier analyses for the two KIRC groups based on the nomogram score. ( G ) Receiver operator characteristic (ROC) analysis of the nomogram in TCGA cohort

    Journal: Cancer Cell International

    Article Title: Assessing the role of programmed cell death signatures and related gene TOP2A in progression and prognostic prediction of clear cell renal cell carcinoma

    doi: 10.1186/s12935-024-03346-w

    Figure Lengend Snippet: Establishment and assessment of the nomogram survival model. ( A ) Univariate analysis for the clinicopathologic characteristics and PCDs in TCGA cohort. ( B ) Multivariate analysis for the clinicopathologic characteristics and PCDs in TCGA cohort. ( C ) A nomogram was established to predict the prognosis of Kidney Renal Clear Cell Carcinoma (KIRC) patients. ( D ) Calibration plots showing the probability of 1-, 3-, and 5-year overall survival in TCGA cohort. ( E ) Kaplan-Meier analyses for the two KIRC groups based on the nomogram score. ( G ) Receiver operator characteristic (ROC) analysis of the nomogram in TCGA cohort

    Article Snippet: The KIRC cell lines 786-O and ACHN were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques:

    TOP2A is overexpressed in KIRC and associated with poor prognosis. ( A ) Area under the curve (AUC) analysis of seven genes distinguishing KIRC tissue from adjacent non-cancerous tissue; Expression of TOP2A in KIRC tissue and adjacent non-cancerous tissue in ( B ) GSE14994, ( C ) GSE36895, ( D ) GSE40435, ( E ) GSE46699, ( F ) GSE53757, ( G ) GSE66272, ( H ) TCGA cohort. ( I ) Expression analysis of the TOP2A gene at different stages in the TCGA cohort. ( J ) Expression analysis of the TOP2A gene in different grades in the TCGA cohort. ( K ) Expression analysis of the TOP2A gene in different grades in the E-MTAB-1980 cohort. OS analysis of TOP2A in ( L ) TCGA, ( M ) Braun-2020, and ( N ) E-MTAB-1980 cohorts. ( O ) Disease-free survival (DFS) analysis of TOP2A in TCGA cohort. ***, p < 0.001

    Journal: Cancer Cell International

    Article Title: Assessing the role of programmed cell death signatures and related gene TOP2A in progression and prognostic prediction of clear cell renal cell carcinoma

    doi: 10.1186/s12935-024-03346-w

    Figure Lengend Snippet: TOP2A is overexpressed in KIRC and associated with poor prognosis. ( A ) Area under the curve (AUC) analysis of seven genes distinguishing KIRC tissue from adjacent non-cancerous tissue; Expression of TOP2A in KIRC tissue and adjacent non-cancerous tissue in ( B ) GSE14994, ( C ) GSE36895, ( D ) GSE40435, ( E ) GSE46699, ( F ) GSE53757, ( G ) GSE66272, ( H ) TCGA cohort. ( I ) Expression analysis of the TOP2A gene at different stages in the TCGA cohort. ( J ) Expression analysis of the TOP2A gene in different grades in the TCGA cohort. ( K ) Expression analysis of the TOP2A gene in different grades in the E-MTAB-1980 cohort. OS analysis of TOP2A in ( L ) TCGA, ( M ) Braun-2020, and ( N ) E-MTAB-1980 cohorts. ( O ) Disease-free survival (DFS) analysis of TOP2A in TCGA cohort. ***, p < 0.001

    Article Snippet: The KIRC cell lines 786-O and ACHN were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: Expressing

    TOP2A promotes proliferation and metastasis of KIRC cells. RT-PCR detection of TOP2A expression in ( A ) 786-O and ( B ) ACHN cells after knockdown of TOP2A. CCK8 assay to measure changes in proliferation ability after knockdown of TOP2A in ( C ) 786-O and ( D ) ACHN cells. Effect of TOP2A knockdown on ( E ) migration and ( G ) invasion ability of 786-O cells. Effect of TOP2A knockdown on ( F ) migration and ( H ) invasion ability of ACHN cells. Impact of TO P2A knockdown on ( I ) proliferation and ( J ) metastasis of ACHN cells in zebrafish. ns, p > 0.05; *, p < 0.05; **, p < 0.01; ***, p < 0.001

    Journal: Cancer Cell International

    Article Title: Assessing the role of programmed cell death signatures and related gene TOP2A in progression and prognostic prediction of clear cell renal cell carcinoma

    doi: 10.1186/s12935-024-03346-w

    Figure Lengend Snippet: TOP2A promotes proliferation and metastasis of KIRC cells. RT-PCR detection of TOP2A expression in ( A ) 786-O and ( B ) ACHN cells after knockdown of TOP2A. CCK8 assay to measure changes in proliferation ability after knockdown of TOP2A in ( C ) 786-O and ( D ) ACHN cells. Effect of TOP2A knockdown on ( E ) migration and ( G ) invasion ability of 786-O cells. Effect of TOP2A knockdown on ( F ) migration and ( H ) invasion ability of ACHN cells. Impact of TO P2A knockdown on ( I ) proliferation and ( J ) metastasis of ACHN cells in zebrafish. ns, p > 0.05; *, p < 0.05; **, p < 0.01; ***, p < 0.001

    Article Snippet: The KIRC cell lines 786-O and ACHN were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: Reverse Transcription Polymerase Chain Reaction, Expressing, CCK-8 Assay, Migration

    CircPRELID2 expression is increased in RCC tissues and cells. A Cluster heat map of dysregulated circRNAs from 4 pairs of RCC tissues and adjacent normal tissues. B Schematic diagram of the biogenesis of circPRELID2 via back-splicing mechanism. CircPRELID2 expression by qRT-PCR in 52 pairs of clinical RCC tissues and matched healthy tissues ( C ), 29 cases RCC patients with TNM stage I + II and 23 cases patients with stage III ( D ), 30 cases RCC patients with negative lymph node metastasis and 22 cases patients with positive metastasis ( E ), HK2, A498, ACHN, RCC4, 769-P and 786-O cells ( F ). * P < 0.05

    Journal: BMC Urology

    Article Title: CircPRELID2 functions as a promoter of renal cell carcinoma through the miR-22-3p/ETV1 cascade

    doi: 10.1186/s12894-024-01490-z

    Figure Lengend Snippet: CircPRELID2 expression is increased in RCC tissues and cells. A Cluster heat map of dysregulated circRNAs from 4 pairs of RCC tissues and adjacent normal tissues. B Schematic diagram of the biogenesis of circPRELID2 via back-splicing mechanism. CircPRELID2 expression by qRT-PCR in 52 pairs of clinical RCC tissues and matched healthy tissues ( C ), 29 cases RCC patients with TNM stage I + II and 23 cases patients with stage III ( D ), 30 cases RCC patients with negative lymph node metastasis and 22 cases patients with positive metastasis ( E ), HK2, A498, ACHN, RCC4, 769-P and 786-O cells ( F ). * P < 0.05

    Article Snippet: Human proximal renal tubular epithelial HK2 cells (ATCC, Rockville, MD, USA) were reproduced in DMEM/F-12 (Life Technologies, Lucerne, Switzerland), and human RCC cell lines A498, ACHN, 769-P and 786-O (ATCC) and RCC4 (Bnbio, Beijing, China) were maintained in 10% FBS RPMI-1640 medium (Life Technologies) plus 1% antibiotics (Life Technologies) in 5% CO 2 at 37 °C.

    Techniques: Expressing, Quantitative RT-PCR

    CircPRELID2 is identified in RCC cells. A and B The expression levels of circPRELID2 by qRT-PCR in both RCC4 and 786-O cells treated with Actinomycin D for 4, 8, 12 and 24 h ( A ), in total RNA digested with RNase R for 15 min ( B ). C CircPRELID2 level by qRT-PCR in cytoplasm and nuclear fraction of RCC4 and 786-O cells, with U6 and 18S rRNA as internal controls. * P < 0.05

    Journal: BMC Urology

    Article Title: CircPRELID2 functions as a promoter of renal cell carcinoma through the miR-22-3p/ETV1 cascade

    doi: 10.1186/s12894-024-01490-z

    Figure Lengend Snippet: CircPRELID2 is identified in RCC cells. A and B The expression levels of circPRELID2 by qRT-PCR in both RCC4 and 786-O cells treated with Actinomycin D for 4, 8, 12 and 24 h ( A ), in total RNA digested with RNase R for 15 min ( B ). C CircPRELID2 level by qRT-PCR in cytoplasm and nuclear fraction of RCC4 and 786-O cells, with U6 and 18S rRNA as internal controls. * P < 0.05

    Article Snippet: Human proximal renal tubular epithelial HK2 cells (ATCC, Rockville, MD, USA) were reproduced in DMEM/F-12 (Life Technologies, Lucerne, Switzerland), and human RCC cell lines A498, ACHN, 769-P and 786-O (ATCC) and RCC4 (Bnbio, Beijing, China) were maintained in 10% FBS RPMI-1640 medium (Life Technologies) plus 1% antibiotics (Life Technologies) in 5% CO 2 at 37 °C.

    Techniques: Expressing, Quantitative RT-PCR

    CircPRELID2 silencing represses RCC cell malignant phenotypes in vitro and in vivo. A - I RCC4 and 786-O cells were transfected with sh-circPRELID2 or sh-NC, followed by the determination of circPRELID2 level by qRT-PCR after 48 h transfection ( A and B ), cell proliferation by CCK-8 assay after 24, 48 and 72 h transfection ( C and D ), cell colony formation using a standard colony formation assay ( E ), cell cycle progression by flow cytometry after 48 h transfection ( F and G ), cell migration and invasion by transwell assay after 24 h transfection ( H and I ). J - L sh-NC- or sh-circPRELID2-transduced RCC4 cells were injected into nude mice (5 mice each group). After 28 days, xenograft tumors were collected. J Growth curve of the xenografts. K Weight of the xenografts. L Immunohistochemistry for Ki-67 staining in the xenografts. * P < 0.05

    Journal: BMC Urology

    Article Title: CircPRELID2 functions as a promoter of renal cell carcinoma through the miR-22-3p/ETV1 cascade

    doi: 10.1186/s12894-024-01490-z

    Figure Lengend Snippet: CircPRELID2 silencing represses RCC cell malignant phenotypes in vitro and in vivo. A - I RCC4 and 786-O cells were transfected with sh-circPRELID2 or sh-NC, followed by the determination of circPRELID2 level by qRT-PCR after 48 h transfection ( A and B ), cell proliferation by CCK-8 assay after 24, 48 and 72 h transfection ( C and D ), cell colony formation using a standard colony formation assay ( E ), cell cycle progression by flow cytometry after 48 h transfection ( F and G ), cell migration and invasion by transwell assay after 24 h transfection ( H and I ). J - L sh-NC- or sh-circPRELID2-transduced RCC4 cells were injected into nude mice (5 mice each group). After 28 days, xenograft tumors were collected. J Growth curve of the xenografts. K Weight of the xenografts. L Immunohistochemistry for Ki-67 staining in the xenografts. * P < 0.05

    Article Snippet: Human proximal renal tubular epithelial HK2 cells (ATCC, Rockville, MD, USA) were reproduced in DMEM/F-12 (Life Technologies, Lucerne, Switzerland), and human RCC cell lines A498, ACHN, 769-P and 786-O (ATCC) and RCC4 (Bnbio, Beijing, China) were maintained in 10% FBS RPMI-1640 medium (Life Technologies) plus 1% antibiotics (Life Technologies) in 5% CO 2 at 37 °C.

    Techniques: In Vitro, In Vivo, Transfection, Quantitative RT-PCR, CCK-8 Assay, Colony Assay, Flow Cytometry, Migration, Transwell Assay, Injection, Immunohistochemistry, Staining

    CircPRELID2 acts as a miR-22-3p sponge to regulate ETV1 expression. A and B Cellular lysates of RCC4 and 786-O cells were incubated with anti-Ago2 or anti-IgG antibody, and then circPRELID2 level was detected by qRT-PCR. C Schematic model of the miR-22-3p-binding sites within circPRELID2 and the mutation in the seed sites. D Schematic of illuminating the miR-22-3p-binding sites within the 3’-UTR of ETV1 and mutated miR-22-3p-binding sites. E CircPRELID2 wide-type or mutant-type reporter construct (circPRELID2-WT or circPRELID2-MUT) was introduced into 293 T cells together with miR-22-3p mimic or miR-NC mimic, and then luciferase activity was assessed. F Relative luciferase activity in the cells co-transfected with ETV1 3’-UTR wild-type reporter (ETV1 3’-UTR-WT) or mutant-type reporter (ETV1 3’-UTR-MUT) and miR-NC mimic or miR-22-3p mimic. G MiR-22-3p expression was determined by qRT-PCR in RCC4 and 786-O cells transfected with sh-NC or sh-circPRELID2. H and I qRT-PCR and immunoblotting for ETV1 mRNA and protein levels in the cells transfected with miR-NC mimic or miR-22-3p mimic. J and K ETV1 expression in cells introduced with si-NC, si-circPRELID2, si-circPRELID2 + anti-miR-NC or si-circPRELID2 + anti-miR-22-3p. L MiR-22-3p expression was detected in 52 pairs of clinical RCC tissues and matched healthy tissues. (M and N) ETV1 expression in RCC tissues and matched healthy tissues. O - Q Expression correlations among miR-22-3p, circPRELID2, ETV1 were tested in RCC tissues using Spearman test. R MiR-22-3p expression was detected in HK2, RCC4 and 786-O cells. S ETV1 protein expression in HK2, RCC4 and 786-O cells. * P < 0.05

    Journal: BMC Urology

    Article Title: CircPRELID2 functions as a promoter of renal cell carcinoma through the miR-22-3p/ETV1 cascade

    doi: 10.1186/s12894-024-01490-z

    Figure Lengend Snippet: CircPRELID2 acts as a miR-22-3p sponge to regulate ETV1 expression. A and B Cellular lysates of RCC4 and 786-O cells were incubated with anti-Ago2 or anti-IgG antibody, and then circPRELID2 level was detected by qRT-PCR. C Schematic model of the miR-22-3p-binding sites within circPRELID2 and the mutation in the seed sites. D Schematic of illuminating the miR-22-3p-binding sites within the 3’-UTR of ETV1 and mutated miR-22-3p-binding sites. E CircPRELID2 wide-type or mutant-type reporter construct (circPRELID2-WT or circPRELID2-MUT) was introduced into 293 T cells together with miR-22-3p mimic or miR-NC mimic, and then luciferase activity was assessed. F Relative luciferase activity in the cells co-transfected with ETV1 3’-UTR wild-type reporter (ETV1 3’-UTR-WT) or mutant-type reporter (ETV1 3’-UTR-MUT) and miR-NC mimic or miR-22-3p mimic. G MiR-22-3p expression was determined by qRT-PCR in RCC4 and 786-O cells transfected with sh-NC or sh-circPRELID2. H and I qRT-PCR and immunoblotting for ETV1 mRNA and protein levels in the cells transfected with miR-NC mimic or miR-22-3p mimic. J and K ETV1 expression in cells introduced with si-NC, si-circPRELID2, si-circPRELID2 + anti-miR-NC or si-circPRELID2 + anti-miR-22-3p. L MiR-22-3p expression was detected in 52 pairs of clinical RCC tissues and matched healthy tissues. (M and N) ETV1 expression in RCC tissues and matched healthy tissues. O - Q Expression correlations among miR-22-3p, circPRELID2, ETV1 were tested in RCC tissues using Spearman test. R MiR-22-3p expression was detected in HK2, RCC4 and 786-O cells. S ETV1 protein expression in HK2, RCC4 and 786-O cells. * P < 0.05

    Article Snippet: Human proximal renal tubular epithelial HK2 cells (ATCC, Rockville, MD, USA) were reproduced in DMEM/F-12 (Life Technologies, Lucerne, Switzerland), and human RCC cell lines A498, ACHN, 769-P and 786-O (ATCC) and RCC4 (Bnbio, Beijing, China) were maintained in 10% FBS RPMI-1640 medium (Life Technologies) plus 1% antibiotics (Life Technologies) in 5% CO 2 at 37 °C.

    Techniques: Expressing, Incubation, Quantitative RT-PCR, Binding Assay, Mutagenesis, Construct, Luciferase, Activity Assay, Transfection, Western Blot

    CircPRELID2 silencing suppresses RCC cell malignant phenotypes by the miR-22-3p/ETV1 axis. A - H RCC4 and 786-O cells were transfected with sh-NC, sh-circPRELID2, sh-circPRELID2 + anti-miR-22-3p or sh-circPRELID2 + OE-ETV1. A Immunoblotting for ETV1 protein expression in the transfected cells. B and C Cell proliferation was assessed. D Cell colony formation using a standard colony formation assay. E and F Cell cycle progression by flow cytometry after 48 h transfection. G and H cell migration and invasion by transwell assay after 24 h transfection. I - L The culture media of transfected cells were collected and used to treat THP-1 monocytic leukemia cells co-treated with 100 ng/mL PMA (Sigma-Aldrich) for macrophage (THP1-M0) induction. After 24 h, the cells were assayed. I Flow cytometry for the CD206 + macrophages. J - L qRT-PCR for mRNA expression of Arg-1, IL-10 and TGF-β1. * P < 0.05

    Journal: BMC Urology

    Article Title: CircPRELID2 functions as a promoter of renal cell carcinoma through the miR-22-3p/ETV1 cascade

    doi: 10.1186/s12894-024-01490-z

    Figure Lengend Snippet: CircPRELID2 silencing suppresses RCC cell malignant phenotypes by the miR-22-3p/ETV1 axis. A - H RCC4 and 786-O cells were transfected with sh-NC, sh-circPRELID2, sh-circPRELID2 + anti-miR-22-3p or sh-circPRELID2 + OE-ETV1. A Immunoblotting for ETV1 protein expression in the transfected cells. B and C Cell proliferation was assessed. D Cell colony formation using a standard colony formation assay. E and F Cell cycle progression by flow cytometry after 48 h transfection. G and H cell migration and invasion by transwell assay after 24 h transfection. I - L The culture media of transfected cells were collected and used to treat THP-1 monocytic leukemia cells co-treated with 100 ng/mL PMA (Sigma-Aldrich) for macrophage (THP1-M0) induction. After 24 h, the cells were assayed. I Flow cytometry for the CD206 + macrophages. J - L qRT-PCR for mRNA expression of Arg-1, IL-10 and TGF-β1. * P < 0.05

    Article Snippet: Human proximal renal tubular epithelial HK2 cells (ATCC, Rockville, MD, USA) were reproduced in DMEM/F-12 (Life Technologies, Lucerne, Switzerland), and human RCC cell lines A498, ACHN, 769-P and 786-O (ATCC) and RCC4 (Bnbio, Beijing, China) were maintained in 10% FBS RPMI-1640 medium (Life Technologies) plus 1% antibiotics (Life Technologies) in 5% CO 2 at 37 °C.

    Techniques: Transfection, Western Blot, Expressing, Colony Assay, Flow Cytometry, Migration, Transwell Assay, Quantitative RT-PCR