hct-8 cells  (CLS Cell Lines Service GmbH)


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    CLS Cell Lines Service GmbH hct-8 cells
    Hct 8 Cells, supplied by CLS Cell Lines Service GmbH, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    hct-8 cells  (CLS Cell Lines Service GmbH)


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    CLS Cell Lines Service GmbH hct-8 cells
    Hct 8 Cells, supplied by CLS Cell Lines Service GmbH, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    hct  (CLS Cell Lines Service GmbH)


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    CLS Cell Lines Service GmbH hct
    Hct, supplied by CLS Cell Lines Service GmbH, 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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    hct  (CLS Cell Lines Service GmbH)


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    CLS Cell Lines Service GmbH hct
    A Cell expansion of lentivirally transduced SW480 or (B) <t>HCT-116</t> cells with two independent shRNAs against TGM2 (shTGM2-1, shTGM2-2) or control (shSCRMBL). C Cell expansion of SW480 and (D) HCT-116 cells after transduction with CRISPR/Cas9 constructs (TGM2 gRNA) against TGM2 or non-target (NT) control. E Mean number of tumorspheres after TGM2 knockdown in SW480 and HCT-116 cells. Data are presented as mean ± SD of at least three independent experiments. F Representative microphotographs of tumorspheres of SW480 cells 14 days after transduction with shTGM2-1, shTGM2-2, or control (shSCRMBL). Shown are fluorescent (tdTOMATO) and brightfield microphotographs. Scale bar, 200 µm. * P < 0.05; ** P < 0.01, Mann–Whitney U test.
    Hct, supplied by CLS Cell Lines Service GmbH, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Transglutaminase 2 promotes tumorigenicity of colon cancer cells by inactivation of the tumor suppressor p53"

    Article Title: Transglutaminase 2 promotes tumorigenicity of colon cancer cells by inactivation of the tumor suppressor p53

    Journal: Oncogene

    doi: 10.1038/s41388-021-01847-w

    A Cell expansion of lentivirally transduced SW480 or (B) HCT-116 cells with two independent shRNAs against TGM2 (shTGM2-1, shTGM2-2) or control (shSCRMBL). C Cell expansion of SW480 and (D) HCT-116 cells after transduction with CRISPR/Cas9 constructs (TGM2 gRNA) against TGM2 or non-target (NT) control. E Mean number of tumorspheres after TGM2 knockdown in SW480 and HCT-116 cells. Data are presented as mean ± SD of at least three independent experiments. F Representative microphotographs of tumorspheres of SW480 cells 14 days after transduction with shTGM2-1, shTGM2-2, or control (shSCRMBL). Shown are fluorescent (tdTOMATO) and brightfield microphotographs. Scale bar, 200 µm. * P < 0.05; ** P < 0.01, Mann–Whitney U test.
    Figure Legend Snippet: A Cell expansion of lentivirally transduced SW480 or (B) HCT-116 cells with two independent shRNAs against TGM2 (shTGM2-1, shTGM2-2) or control (shSCRMBL). C Cell expansion of SW480 and (D) HCT-116 cells after transduction with CRISPR/Cas9 constructs (TGM2 gRNA) against TGM2 or non-target (NT) control. E Mean number of tumorspheres after TGM2 knockdown in SW480 and HCT-116 cells. Data are presented as mean ± SD of at least three independent experiments. F Representative microphotographs of tumorspheres of SW480 cells 14 days after transduction with shTGM2-1, shTGM2-2, or control (shSCRMBL). Shown are fluorescent (tdTOMATO) and brightfield microphotographs. Scale bar, 200 µm. * P < 0.05; ** P < 0.01, Mann–Whitney U test.

    Techniques Used: Transduction, CRISPR, Construct, MANN-WHITNEY

    A Time-lapse imaging of SW480 cells transduced with shTGM2-1, shTGM2-2 or shSCRMBL. Shown are cumulative cell death events over time determined by single cell tracking. P value was calculated by log-rank test. B Percentage of apoptotic SW480 cells determined by Annexin V/7-AAD staining 72 hours after TGM2 knockdown. C Percentage of Caspase-3 positive SW480 cells 72 hours after TGM2 knockdown. D – F All experiments were repeated in HCT-116 cells transduced with shTGM2-1, shTGM2-2 or shSCRMBL. D Time lapse imaging showing the cumulative cell death events. E Percentage of Annexin V positive and ( F) Caspase-3 positive HCT-116 cells 72 hours after TGM2 knockdown. Results are presented as mean ± SD of three independent experiments. *** P < 0.001, Mann–Whitney U test.
    Figure Legend Snippet: A Time-lapse imaging of SW480 cells transduced with shTGM2-1, shTGM2-2 or shSCRMBL. Shown are cumulative cell death events over time determined by single cell tracking. P value was calculated by log-rank test. B Percentage of apoptotic SW480 cells determined by Annexin V/7-AAD staining 72 hours after TGM2 knockdown. C Percentage of Caspase-3 positive SW480 cells 72 hours after TGM2 knockdown. D – F All experiments were repeated in HCT-116 cells transduced with shTGM2-1, shTGM2-2 or shSCRMBL. D Time lapse imaging showing the cumulative cell death events. E Percentage of Annexin V positive and ( F) Caspase-3 positive HCT-116 cells 72 hours after TGM2 knockdown. Results are presented as mean ± SD of three independent experiments. *** P < 0.001, Mann–Whitney U test.

    Techniques Used: Imaging, Transduction, Single Cell Tracking, Staining, MANN-WHITNEY

    A – C Gene expression profiling by RNA-seq of SW480 cells after transduction with either shTGM2-1 or shSCRMBL. A Unsupervised hierarchical clustering of the top 1000 differentially expressed genes (DEGs) upon TGM2 knockdown across the four biological replicates. B MA plot relating p values for all differentially expressed genes between shTGM2-1 and shSCRMBL from four biological replicates. Red dots indicate significantly regulated genes (adjusted P < 0.05). List of regulated genes is presented in Supplementary Table S . C Scatter plot of gene set enrichment analysis of DEGs relating the Q-value for Hallmark gene-set signatures. The top 16 enriched pathways are shown ( P < 0.05, Fold change ≥2). The color and size of each dot represent the Rich factor and the number of DEGs mapped to the indicated pathway, respectively. D Proteome analysis of regulated proteins involved in apoptosis upon shRNA-mediated TGM2 knockdown. Representative blot of Proteome Profiler Array™-Human Apoptosis Array analysis of SW480 cells. The regulation of protein expression of phosphorylated p53 variants is shown. E – H Quantification of p53 and phosphorylated p53 (S15, S46, and S392) upon TGM2 knockdown in SW480 ( E , G ) and HCT-116 ( F , H ) cells via Simple Western technology ( n = 3; Mann–Whitney U test).
    Figure Legend Snippet: A – C Gene expression profiling by RNA-seq of SW480 cells after transduction with either shTGM2-1 or shSCRMBL. A Unsupervised hierarchical clustering of the top 1000 differentially expressed genes (DEGs) upon TGM2 knockdown across the four biological replicates. B MA plot relating p values for all differentially expressed genes between shTGM2-1 and shSCRMBL from four biological replicates. Red dots indicate significantly regulated genes (adjusted P < 0.05). List of regulated genes is presented in Supplementary Table S . C Scatter plot of gene set enrichment analysis of DEGs relating the Q-value for Hallmark gene-set signatures. The top 16 enriched pathways are shown ( P < 0.05, Fold change ≥2). The color and size of each dot represent the Rich factor and the number of DEGs mapped to the indicated pathway, respectively. D Proteome analysis of regulated proteins involved in apoptosis upon shRNA-mediated TGM2 knockdown. Representative blot of Proteome Profiler Array™-Human Apoptosis Array analysis of SW480 cells. The regulation of protein expression of phosphorylated p53 variants is shown. E – H Quantification of p53 and phosphorylated p53 (S15, S46, and S392) upon TGM2 knockdown in SW480 ( E , G ) and HCT-116 ( F , H ) cells via Simple Western technology ( n = 3; Mann–Whitney U test).

    Techniques Used: Expressing, RNA Sequencing Assay, Transduction, shRNA, Western Blot, MANN-WHITNEY

    A Representative images of proximity ligation assay (PLA) of TGM2 and p53 in SW480 cells. Cells incubated only with TGM2 antibody served as negative control (I). Protein–protein interaction of TGM2 and p53(S15) was visualized using hybridization probes labeled with Texas Red (II). Nuclei were stained with DAPI (blue). B Quantification of TGM2-p53 interaction and associated technical controls (Ctrl). Technical controls demonstrate the specificity of PLA signals. Each dot represents one cell. Mean value of PLA dots per cell is shown by the black line. C Representative images of proximity ligation assay of TGM2 and p53 in patient-derived normal epithelial cells (I) and corresponding colon cancer cells (II). D Quantification of TGM2-p53 interaction in primary patient material. (Significance was calculated using Kruskal–Wallis test). E Co-immunoprecipitation (Co-IP) of endogenous TGM2 and p53 or phosphorylated p53(S15) in SW480, HCT-116 p53 wildtype cells (wt) and HCT-116 p53 knockout cells (−/−). F Super-resolved image of a HCT-116 cell immunostained for TGM2 (red) and p53(S15) (cyan). A zoom-in of the highlighted region is shown on the right. White regions indicate overlapping signal of TGM2 and p53(S15) (yellow arrowheads). Scale bars represent 5 µm and 1 µm, respectively.
    Figure Legend Snippet: A Representative images of proximity ligation assay (PLA) of TGM2 and p53 in SW480 cells. Cells incubated only with TGM2 antibody served as negative control (I). Protein–protein interaction of TGM2 and p53(S15) was visualized using hybridization probes labeled with Texas Red (II). Nuclei were stained with DAPI (blue). B Quantification of TGM2-p53 interaction and associated technical controls (Ctrl). Technical controls demonstrate the specificity of PLA signals. Each dot represents one cell. Mean value of PLA dots per cell is shown by the black line. C Representative images of proximity ligation assay of TGM2 and p53 in patient-derived normal epithelial cells (I) and corresponding colon cancer cells (II). D Quantification of TGM2-p53 interaction in primary patient material. (Significance was calculated using Kruskal–Wallis test). E Co-immunoprecipitation (Co-IP) of endogenous TGM2 and p53 or phosphorylated p53(S15) in SW480, HCT-116 p53 wildtype cells (wt) and HCT-116 p53 knockout cells (−/−). F Super-resolved image of a HCT-116 cell immunostained for TGM2 (red) and p53(S15) (cyan). A zoom-in of the highlighted region is shown on the right. White regions indicate overlapping signal of TGM2 and p53(S15) (yellow arrowheads). Scale bars represent 5 µm and 1 µm, respectively.

    Techniques Used: Proximity Ligation Assay, Incubation, Negative Control, Hybridization, Labeling, Staining, Derivative Assay, Immunoprecipitation, Co-Immunoprecipitation Assay, Knock-Out

    A – C HCT-116 p53 wildtype cells (wt) and HCT-116 p53 knockout cells (−/−) were transduced with either shTGM2-1, shTGM2-2, or shSCRMBL. Time-lapse imaging and proliferation assay were performed to determine a rescue from cell death upon TGM2 knockdown. A Fold change of cell number of HCT-116 p53 wt and HCT-116 p53 −/− cells upon TGM2 knockdown in comparison to shSCRMBL control determined at day three after transduction. Data are presented as mean ± SD of three independent experiments (** P < 0.01, Mann–Whitney U test). B Single cell tracking of HCT-116 p53 wt and HCT-116 p53 − /− cells after TGM2 knockdown with shTGM2-1 and (C) shTGM2-2. Cumulative cell death events are shown over time (*** P < 0.001, Log-rank test). D Direct visualization of p53 activation upon TGM2 knockdown by time-lapse video-microscopy. Sequence of phase contrast images, tdTOMATO fluorescence of shTGM2-1 and p53-driven destabilized GFP reporter , depicting the same field of view over the time course of 30 hours as indicated in the corresponding panels in I–VIII. The yellow circles designate tracked cells over time. (I–VIII) show corresponding sequence of fluorescence images taken at the same time points as the phase contrast images. (I) Shown are two representative HCT-116 cells. (II and III) 6-8 hours after lentiviral transduction of shTGM2-1 both HCT-116 cells express the red fluorescent tdTOMATO reporter, indicating a knockdown of TGM2. (IV-VI) Another 4–10 hours later both cells express the green fluorescent (GFP) p53 reporter, indicating the induction of p53 activity. (VII and VIII) About 24 hours after transduction both HCT-116 cells subsequently undergo apoptosis (white arrows). Movie S shows all assembled images (3 min temporal resolution) of the same sequence.
    Figure Legend Snippet: A – C HCT-116 p53 wildtype cells (wt) and HCT-116 p53 knockout cells (−/−) were transduced with either shTGM2-1, shTGM2-2, or shSCRMBL. Time-lapse imaging and proliferation assay were performed to determine a rescue from cell death upon TGM2 knockdown. A Fold change of cell number of HCT-116 p53 wt and HCT-116 p53 −/− cells upon TGM2 knockdown in comparison to shSCRMBL control determined at day three after transduction. Data are presented as mean ± SD of three independent experiments (** P < 0.01, Mann–Whitney U test). B Single cell tracking of HCT-116 p53 wt and HCT-116 p53 − /− cells after TGM2 knockdown with shTGM2-1 and (C) shTGM2-2. Cumulative cell death events are shown over time (*** P < 0.001, Log-rank test). D Direct visualization of p53 activation upon TGM2 knockdown by time-lapse video-microscopy. Sequence of phase contrast images, tdTOMATO fluorescence of shTGM2-1 and p53-driven destabilized GFP reporter , depicting the same field of view over the time course of 30 hours as indicated in the corresponding panels in I–VIII. The yellow circles designate tracked cells over time. (I–VIII) show corresponding sequence of fluorescence images taken at the same time points as the phase contrast images. (I) Shown are two representative HCT-116 cells. (II and III) 6-8 hours after lentiviral transduction of shTGM2-1 both HCT-116 cells express the red fluorescent tdTOMATO reporter, indicating a knockdown of TGM2. (IV-VI) Another 4–10 hours later both cells express the green fluorescent (GFP) p53 reporter, indicating the induction of p53 activity. (VII and VIII) About 24 hours after transduction both HCT-116 cells subsequently undergo apoptosis (white arrows). Movie S shows all assembled images (3 min temporal resolution) of the same sequence.

    Techniques Used: Knock-Out, Transduction, Imaging, Proliferation Assay, MANN-WHITNEY, Single Cell Tracking, Activation Assay, Microscopy, Sequencing, Fluorescence, Activity Assay

    hct 116  (CLS Cell Lines Service GmbH)


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    CLS Cell Lines Service GmbH hct 116
    Hct 116, supplied by CLS Cell Lines Service GmbH, 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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    hct-15 cells  (CLS Cell Lines Service GmbH)


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    CLS Cell Lines Service GmbH hct-15 cells
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    hct 15  (CLS Cell Lines Service GmbH)


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    CLS Cell Lines Service GmbH hct 15
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    hct 116  (CLS Cell Lines Service GmbH)


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    CLS Cell Lines Service GmbH hct 116
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    hct 116  (CLS Cell Lines Service GmbH)


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    CLS Cell Lines Service GmbH hct 116
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    hct 116  (CLS Cell Lines Service GmbH)


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    CLS Cell Lines Service GmbH hct 116
    Antiproliferative activity of compounds 6 ( a – e ) and 9 ( a – n ) on six representative tumor cell lines.
    Hct 116, supplied by CLS Cell Lines Service GmbH, 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 "Synthetic Development of New 3-(4-Arylmethylamino)butyl-5-arylidene-rhodanines under Microwave Irradiation and Their Effects on Tumor Cell Lines and against Protein Kinases"

    Article Title: Synthetic Development of New 3-(4-Arylmethylamino)butyl-5-arylidene-rhodanines under Microwave Irradiation and Their Effects on Tumor Cell Lines and against Protein Kinases

    Journal: Molecules

    doi: 10.3390/molecules200712412

    Antiproliferative activity of compounds 6 ( a – e ) and 9 ( a – n ) on six representative tumor cell lines.
    Figure Legend Snippet: Antiproliferative activity of compounds 6 ( a – e ) and 9 ( a – n ) on six representative tumor cell lines.

    Techniques Used: Activity Assay

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