colorectal cancer cell lines dld 1  (ATCC)


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    ATCC colorectal cancer cell lines dld 1
    Colorectal Cancer Cell Lines Dld 1, supplied by ATCC, 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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    colorectal cancer cell lines dld 1  (ATCC)


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    ATCC colorectal cancer cell lines dld 1
    Colorectal Cancer Cell Lines Dld 1, supplied by ATCC, 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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    human colorectal cancer cell lines dld 1  (ATCC)


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    ATCC human colorectal cancer cell lines dld 1
    Intestinal Dot1l affects the Wnt/β-catenin pathway. (a) Wnt/β-catenin downstream genes mRNA expression from Dot1l FF and Dot1l ΔIEC mice day 70 of the colorectal cancer model, n = 7–8, ** P = .0069 for Axin2 , **** P < .0001 for Sox4 , ** P = .0038 for Lgr5 , *** P = .0006 for Ephb3 , Student’s t-test. (b) Western blot of Axin2 expression from Dot1l FF and Dot1l ΔIEC mice day 70 of the colorectal cancer model. One of three is shown. (c) Immunofluorescence staining of β-catenin and Axin2 in Dot1l FF and Dot1l ΔIEC colorectal on day 14 of AOM-DSS model. Green: β-catenin, Red: Axin2, Blue: DAPI. (d and e) Effect of EPZ004777 on Wnt/β-catenin downstream gene mRNA expression in <t>DLD-1</t> (d) and HT29 (e) cells. (d) ** P = .0023 for AXIN2 , ** P = .0026 for SOX4 , * P = .0475 for EPHB3 , ** P = .0026 for LGR5 . (e) ** P = .0081 for AXIN2 , ** P = .0046 for SOX4 , ** P = .007 for EPHB3 . Student’s t-test. (f and g) Effect of DOT1L knockdown on Wnt/β-catenin downstream gene mRNA expression in DLD-1 (f) and HT29 (g) cells. (f) * P < .05 . (g) ** P = .0081 for AXIN2 , ** P = .0046 for SOX4 , ** P = .007 for EPHB3 , Student’s t-test. (h and i) H3K79me2 ChIP on the promoter (p) and different gene body regions (B1, B2, and B3) of SOX4 (h) and AXIN2 (i) in DLD-1 cells. NS, P > .05, * P ≤ .05, ** P ≤ .01, *** P ≤ .001, **** P ≤ .0001 , one-way ANOVA.
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    1) Product Images from "DOT1L affects colorectal carcinogenesis via altering T cell subsets and oncogenic pathway"

    Article Title: DOT1L affects colorectal carcinogenesis via altering T cell subsets and oncogenic pathway

    Journal: Oncoimmunology

    doi: 10.1080/2162402X.2022.2052640

    Intestinal Dot1l affects the Wnt/β-catenin pathway. (a) Wnt/β-catenin downstream genes mRNA expression from Dot1l FF and Dot1l ΔIEC mice day 70 of the colorectal cancer model, n = 7–8, ** P = .0069 for Axin2 , **** P < .0001 for Sox4 , ** P = .0038 for Lgr5 , *** P = .0006 for Ephb3 , Student’s t-test. (b) Western blot of Axin2 expression from Dot1l FF and Dot1l ΔIEC mice day 70 of the colorectal cancer model. One of three is shown. (c) Immunofluorescence staining of β-catenin and Axin2 in Dot1l FF and Dot1l ΔIEC colorectal on day 14 of AOM-DSS model. Green: β-catenin, Red: Axin2, Blue: DAPI. (d and e) Effect of EPZ004777 on Wnt/β-catenin downstream gene mRNA expression in DLD-1 (d) and HT29 (e) cells. (d) ** P = .0023 for AXIN2 , ** P = .0026 for SOX4 , * P = .0475 for EPHB3 , ** P = .0026 for LGR5 . (e) ** P = .0081 for AXIN2 , ** P = .0046 for SOX4 , ** P = .007 for EPHB3 . Student’s t-test. (f and g) Effect of DOT1L knockdown on Wnt/β-catenin downstream gene mRNA expression in DLD-1 (f) and HT29 (g) cells. (f) * P < .05 . (g) ** P = .0081 for AXIN2 , ** P = .0046 for SOX4 , ** P = .007 for EPHB3 , Student’s t-test. (h and i) H3K79me2 ChIP on the promoter (p) and different gene body regions (B1, B2, and B3) of SOX4 (h) and AXIN2 (i) in DLD-1 cells. NS, P > .05, * P ≤ .05, ** P ≤ .01, *** P ≤ .001, **** P ≤ .0001 , one-way ANOVA.
    Figure Legend Snippet: Intestinal Dot1l affects the Wnt/β-catenin pathway. (a) Wnt/β-catenin downstream genes mRNA expression from Dot1l FF and Dot1l ΔIEC mice day 70 of the colorectal cancer model, n = 7–8, ** P = .0069 for Axin2 , **** P < .0001 for Sox4 , ** P = .0038 for Lgr5 , *** P = .0006 for Ephb3 , Student’s t-test. (b) Western blot of Axin2 expression from Dot1l FF and Dot1l ΔIEC mice day 70 of the colorectal cancer model. One of three is shown. (c) Immunofluorescence staining of β-catenin and Axin2 in Dot1l FF and Dot1l ΔIEC colorectal on day 14 of AOM-DSS model. Green: β-catenin, Red: Axin2, Blue: DAPI. (d and e) Effect of EPZ004777 on Wnt/β-catenin downstream gene mRNA expression in DLD-1 (d) and HT29 (e) cells. (d) ** P = .0023 for AXIN2 , ** P = .0026 for SOX4 , * P = .0475 for EPHB3 , ** P = .0026 for LGR5 . (e) ** P = .0081 for AXIN2 , ** P = .0046 for SOX4 , ** P = .007 for EPHB3 . Student’s t-test. (f and g) Effect of DOT1L knockdown on Wnt/β-catenin downstream gene mRNA expression in DLD-1 (f) and HT29 (g) cells. (f) * P < .05 . (g) ** P = .0081 for AXIN2 , ** P = .0046 for SOX4 , ** P = .007 for EPHB3 , Student’s t-test. (h and i) H3K79me2 ChIP on the promoter (p) and different gene body regions (B1, B2, and B3) of SOX4 (h) and AXIN2 (i) in DLD-1 cells. NS, P > .05, * P ≤ .05, ** P ≤ .01, *** P ≤ .001, **** P ≤ .0001 , one-way ANOVA.

    Techniques Used: Expressing, Western Blot, Immunofluorescence, Staining

    colorectal cancer cell lines dld 1  (ATCC)


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    ATCC colorectal cancer cell lines dld 1
    Knockout of Human endogenous retroviruse (HERV)-K env gene in <t>DLD-1</t> colorectal cancer cells. ( a ) Knockout of HERV-K env gene in HERV-K119 region. Genomic polymerase chain reaction (PCR) was performed for specific regions of HERV-K env derivatives. ( b ) Expression of HERV-K env RNA in HERV-K env knockout (KO) and over-expressing DLD-1 colorectal cancer cells. RT-PCR performed for general region of HERV-K env gene. ( c ) Expression of HERV-K119 gag, pro, pol, and rec genes in DLD-1 colorectal cancer cells ( d ) Expression of HERV-K Env protein in HERV-K env KO and over-expressing DLD-1 colorectal cancer cells. Western blot was performed to analyze the protein level of HERV-K Env. ( e ) Immunofluorescence and immunohistochemical staining of the HERV-K Env expression in colorectal cancer cells. HERV-K env gene in HERV-K119 region was completely deleted and the expression of RNA and protein level of HERV-K env gene was significantly reduced. The expression of glucose 6 phosphate dehydrogenase (GAPDH) was served as a loading control. (−: KO, +: over-expression).
    Colorectal Cancer Cell Lines Dld 1, supplied by ATCC, 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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    1) Product Images from "Human Endogenous Retrovirus (HERV)-K env Gene Knockout Affects Tumorigenic Characteristics of nupr1 Gene in DLD-1 Colorectal Cancer Cells"

    Article Title: Human Endogenous Retrovirus (HERV)-K env Gene Knockout Affects Tumorigenic Characteristics of nupr1 Gene in DLD-1 Colorectal Cancer Cells

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms22083941

    Knockout of Human endogenous retroviruse (HERV)-K env gene in DLD-1 colorectal cancer cells. ( a ) Knockout of HERV-K env gene in HERV-K119 region. Genomic polymerase chain reaction (PCR) was performed for specific regions of HERV-K env derivatives. ( b ) Expression of HERV-K env RNA in HERV-K env knockout (KO) and over-expressing DLD-1 colorectal cancer cells. RT-PCR performed for general region of HERV-K env gene. ( c ) Expression of HERV-K119 gag, pro, pol, and rec genes in DLD-1 colorectal cancer cells ( d ) Expression of HERV-K Env protein in HERV-K env KO and over-expressing DLD-1 colorectal cancer cells. Western blot was performed to analyze the protein level of HERV-K Env. ( e ) Immunofluorescence and immunohistochemical staining of the HERV-K Env expression in colorectal cancer cells. HERV-K env gene in HERV-K119 region was completely deleted and the expression of RNA and protein level of HERV-K env gene was significantly reduced. The expression of glucose 6 phosphate dehydrogenase (GAPDH) was served as a loading control. (−: KO, +: over-expression).
    Figure Legend Snippet: Knockout of Human endogenous retroviruse (HERV)-K env gene in DLD-1 colorectal cancer cells. ( a ) Knockout of HERV-K env gene in HERV-K119 region. Genomic polymerase chain reaction (PCR) was performed for specific regions of HERV-K env derivatives. ( b ) Expression of HERV-K env RNA in HERV-K env knockout (KO) and over-expressing DLD-1 colorectal cancer cells. RT-PCR performed for general region of HERV-K env gene. ( c ) Expression of HERV-K119 gag, pro, pol, and rec genes in DLD-1 colorectal cancer cells ( d ) Expression of HERV-K Env protein in HERV-K env KO and over-expressing DLD-1 colorectal cancer cells. Western blot was performed to analyze the protein level of HERV-K Env. ( e ) Immunofluorescence and immunohistochemical staining of the HERV-K Env expression in colorectal cancer cells. HERV-K env gene in HERV-K119 region was completely deleted and the expression of RNA and protein level of HERV-K env gene was significantly reduced. The expression of glucose 6 phosphate dehydrogenase (GAPDH) was served as a loading control. (−: KO, +: over-expression).

    Techniques Used: Knock-Out, Polymerase Chain Reaction, Expressing, Reverse Transcription Polymerase Chain Reaction, Western Blot, Immunofluorescence, Immunohistochemical staining, Staining, Over Expression

    HERV-K env KO reduced tumorigenic characteristics including proliferation, invasion, migration, and tumor colonization in DLD-1 colorectal cancer cells. ( a ) Cell proliferation of HERV-K env KO and over-expressing DLD-1 colorectal cancer cell. Cell proliferation was significantly reduced in HERV-K KO group and increased in over-expression groups of DLD-1 colorectal cancer cells. ( b ) Invasion and migration of HERV-K env KO and over-expressing DLD-1 colorectal cancer cell. Invasion and migration were significantly reduced in HERV-K KO group and increased in over-expression groups of DLD-1 colorectal cancer cells. ( c ) Soft-agar colony forming assay. Colony formation ability on soft agar was significantly reduced in HERV-K KO group and increased in over-expression groups of DLD-1 colorectal cancer cells. * p < 0.05, ** p < 0.01. (−: KO, +: over-expression).
    Figure Legend Snippet: HERV-K env KO reduced tumorigenic characteristics including proliferation, invasion, migration, and tumor colonization in DLD-1 colorectal cancer cells. ( a ) Cell proliferation of HERV-K env KO and over-expressing DLD-1 colorectal cancer cell. Cell proliferation was significantly reduced in HERV-K KO group and increased in over-expression groups of DLD-1 colorectal cancer cells. ( b ) Invasion and migration of HERV-K env KO and over-expressing DLD-1 colorectal cancer cell. Invasion and migration were significantly reduced in HERV-K KO group and increased in over-expression groups of DLD-1 colorectal cancer cells. ( c ) Soft-agar colony forming assay. Colony formation ability on soft agar was significantly reduced in HERV-K KO group and increased in over-expression groups of DLD-1 colorectal cancer cells. * p < 0.05, ** p < 0.01. (−: KO, +: over-expression).

    Techniques Used: Migration, Expressing, Over Expression

    The effect of HERV-K env on in vivo tumor growth. ( a ) Subcutaneous implantation of Mock, HERV-K env KO and over-expressing DLD-1 colorectal cancer cells in nude mice led to tumor formation. ( b ) Tumors from sacrificed mice. Growth curve of xenograft tumors volume of Mock, HERV-K env KO and over-expressing DLD-1 colorectal cancer cells. Tumor size was significantly reduced in HERV-K env KO group and increased in over-expression groups of DLD-1 colorectal cancer cells. p -value was determined by comparing tumor size in Mock group with HERV-K env + or − group. * p < 0.05, ** p < 0.01. (−: KO, +: over-expression).
    Figure Legend Snippet: The effect of HERV-K env on in vivo tumor growth. ( a ) Subcutaneous implantation of Mock, HERV-K env KO and over-expressing DLD-1 colorectal cancer cells in nude mice led to tumor formation. ( b ) Tumors from sacrificed mice. Growth curve of xenograft tumors volume of Mock, HERV-K env KO and over-expressing DLD-1 colorectal cancer cells. Tumor size was significantly reduced in HERV-K env KO group and increased in over-expression groups of DLD-1 colorectal cancer cells. p -value was determined by comparing tumor size in Mock group with HERV-K env + or − group. * p < 0.05, ** p < 0.01. (−: KO, +: over-expression).

    Techniques Used: In Vivo, Expressing, Over Expression

    Transcriptome analysis of Mock, HERV-K env KO, and HERV-K env over-expressing DLD-1 colorectal cancer cells. ( a ) Heatmap of gene expression changes of DLD-1 cells. Differentially expressed genes were classified based on the log2 ratio of expression in Mock to HERV-K env KO or over-expression. The number of up- and down-regulated genes identified from the three comparison groups (CON vs. POE, CON vs. NKO, and POE vs. NKO). Red: upregulation, Blue: downregulation. CON: Control, POE: overexpressed, NKO: knockout. ( b ) Fold changes of HERV-K env KO and over-expressing compared with Mock DLD-1 colorectal cancer cells. (−: KO, +: over-expression).
    Figure Legend Snippet: Transcriptome analysis of Mock, HERV-K env KO, and HERV-K env over-expressing DLD-1 colorectal cancer cells. ( a ) Heatmap of gene expression changes of DLD-1 cells. Differentially expressed genes were classified based on the log2 ratio of expression in Mock to HERV-K env KO or over-expression. The number of up- and down-regulated genes identified from the three comparison groups (CON vs. POE, CON vs. NKO, and POE vs. NKO). Red: upregulation, Blue: downregulation. CON: Control, POE: overexpressed, NKO: knockout. ( b ) Fold changes of HERV-K env KO and over-expressing compared with Mock DLD-1 colorectal cancer cells. (−: KO, +: over-expression).

    Techniques Used: Expressing, Over Expression, Knock-Out

    Protein expression of various target genes regulate by HERV-K env gene. ( a ) RNA expression of HERV-K env gene in HERV-K env KO, over-expressing, and HERV-K env re-expressed (Re-expressed) DLD-1 colorectal cancer cells. ( b ) Protein expression of various target genes regulated by HERV-K env gene. The expression of RB protein was significantly increased in HERV-K env KO groups of DLD-1 colorectal cancer cells. ( c ) Immunohistochemical analysis of NUPR1 protein in HERV-K env KO, over-expressing, and HERV-K env re- expressed DLD-1 colorectal cancer cells. NUPR1 protein level was reduced in HERV-K env KO groups. (−: KO, +: over-expression).
    Figure Legend Snippet: Protein expression of various target genes regulate by HERV-K env gene. ( a ) RNA expression of HERV-K env gene in HERV-K env KO, over-expressing, and HERV-K env re-expressed (Re-expressed) DLD-1 colorectal cancer cells. ( b ) Protein expression of various target genes regulated by HERV-K env gene. The expression of RB protein was significantly increased in HERV-K env KO groups of DLD-1 colorectal cancer cells. ( c ) Immunohistochemical analysis of NUPR1 protein in HERV-K env KO, over-expressing, and HERV-K env re- expressed DLD-1 colorectal cancer cells. NUPR1 protein level was reduced in HERV-K env KO groups. (−: KO, +: over-expression).

    Techniques Used: Expressing, RNA Expression, Immunohistochemical staining, Over Expression

    Effect of NUPR1 on DLD-1 colorectal cancer cells. ( a ) Expression of target genes in the DLD-1 colorectal cancer cells treated with siRNA of nupr1 gene. Western blot analysis shows that the expression of NUPR1 protein was markedly reduced, with RB protein levels markedly induced by silencing of nupr1 gene respectively. ( b ) The effect of nupr1 gene silencing on cell proliferation of DLD-1 colorectal cancer cells. Cell proliferation rate was significantly reduced by treatment with siRNA of nupr1 gene in DLD-1 colorectal cancer cells. ** p < 0.01.
    Figure Legend Snippet: Effect of NUPR1 on DLD-1 colorectal cancer cells. ( a ) Expression of target genes in the DLD-1 colorectal cancer cells treated with siRNA of nupr1 gene. Western blot analysis shows that the expression of NUPR1 protein was markedly reduced, with RB protein levels markedly induced by silencing of nupr1 gene respectively. ( b ) The effect of nupr1 gene silencing on cell proliferation of DLD-1 colorectal cancer cells. Cell proliferation rate was significantly reduced by treatment with siRNA of nupr1 gene in DLD-1 colorectal cancer cells. ** p < 0.01.

    Techniques Used: Expressing, Western Blot

    A schematic diagram on the pathways related to the HERV-K env KO. HERV-K env KO reduced the protein level of NUPR1, and its signaling activates the RB tumor suppressor gene to reduce the cell proliferation of DLD-1 colorectal cancer. (−: KO, +: over-expression).
    Figure Legend Snippet: A schematic diagram on the pathways related to the HERV-K env KO. HERV-K env KO reduced the protein level of NUPR1, and its signaling activates the RB tumor suppressor gene to reduce the cell proliferation of DLD-1 colorectal cancer. (−: KO, +: over-expression).

    Techniques Used: Over Expression

    human colorectal cancer cell lines dld 1  (ATCC)


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    ATCC human colorectal cancer cell lines dld 1
    PCBP1 Overexpression represses autophagy. (A) Immunoblots of PCBP1, LC3B I and II in PCBP1-overexpression (GFP-PCBP1) and the GFP control cells. β-actin is used as an internal loading control. (B) Immunofluorescence staining of LC3B puncta in both A2780 and <t>DLD-1</t> cells with or without CQ treatment for 24 h. GFP-PCBP1 cells are in green, while parent control cell are not green. Cells counterstained with DAPI are shown in blue. White arrows point LC3B puncta (Red) in the parental control cells without GFP-PCBP1 transfection (not green), while the red arrows point LC3B puncta in GFP-PCBP1-transfected cells (green). Bars equal to 25 μm. (C) Quantifications of LC3B puncta intensity per cell in B are presented as histograms (mean ± SD). Parent group indicates the parent control cells without GFP-PCBP1 (not green), while the PCBP1 group indicates the cells with transfected GFP-PCBP1 (green). ** P < 0.01; *** P < 0.001, n = 5. (D) Immunoblots of LC3B I, II in A2780 and DLD-1 cells with PCBP1 and GFP overexpression. Upon CQ or DMSO (control) treatment for 24 h, cells were analyzed. Immunoblot intensity ratio of LC3B II to GAPDH were, respectively, quantified and normalized, and indicated in each lane. (E) Immunofluorescence staining of LC3B puncta in both A2780 and DLD-1 cells with or without CQ treatment for 24 h. PCBP1 knockdown (KD) cells are in green, while parent control cells are not green. Cells counterstained with DAPI are in blue. White arrows point LC3B puncta (Red) in the PCBP1 KD cells, while the red arrows point LC3B puncta in the parental control cells. Scale bars in (B,E) equal to 25 μm.
    Human Colorectal Cancer Cell Lines Dld 1, supplied by ATCC, 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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    1) Product Images from "Poly C Binding Protein 1 Regulates p62/SQSTM1 mRNA Stability and Autophagic Degradation to Repress Tumor Progression"

    Article Title: Poly C Binding Protein 1 Regulates p62/SQSTM1 mRNA Stability and Autophagic Degradation to Repress Tumor Progression

    Journal: Frontiers in Genetics

    doi: 10.3389/fgene.2020.00930

    PCBP1 Overexpression represses autophagy. (A) Immunoblots of PCBP1, LC3B I and II in PCBP1-overexpression (GFP-PCBP1) and the GFP control cells. β-actin is used as an internal loading control. (B) Immunofluorescence staining of LC3B puncta in both A2780 and DLD-1 cells with or without CQ treatment for 24 h. GFP-PCBP1 cells are in green, while parent control cell are not green. Cells counterstained with DAPI are shown in blue. White arrows point LC3B puncta (Red) in the parental control cells without GFP-PCBP1 transfection (not green), while the red arrows point LC3B puncta in GFP-PCBP1-transfected cells (green). Bars equal to 25 μm. (C) Quantifications of LC3B puncta intensity per cell in B are presented as histograms (mean ± SD). Parent group indicates the parent control cells without GFP-PCBP1 (not green), while the PCBP1 group indicates the cells with transfected GFP-PCBP1 (green). ** P < 0.01; *** P < 0.001, n = 5. (D) Immunoblots of LC3B I, II in A2780 and DLD-1 cells with PCBP1 and GFP overexpression. Upon CQ or DMSO (control) treatment for 24 h, cells were analyzed. Immunoblot intensity ratio of LC3B II to GAPDH were, respectively, quantified and normalized, and indicated in each lane. (E) Immunofluorescence staining of LC3B puncta in both A2780 and DLD-1 cells with or without CQ treatment for 24 h. PCBP1 knockdown (KD) cells are in green, while parent control cells are not green. Cells counterstained with DAPI are in blue. White arrows point LC3B puncta (Red) in the PCBP1 KD cells, while the red arrows point LC3B puncta in the parental control cells. Scale bars in (B,E) equal to 25 μm.
    Figure Legend Snippet: PCBP1 Overexpression represses autophagy. (A) Immunoblots of PCBP1, LC3B I and II in PCBP1-overexpression (GFP-PCBP1) and the GFP control cells. β-actin is used as an internal loading control. (B) Immunofluorescence staining of LC3B puncta in both A2780 and DLD-1 cells with or without CQ treatment for 24 h. GFP-PCBP1 cells are in green, while parent control cell are not green. Cells counterstained with DAPI are shown in blue. White arrows point LC3B puncta (Red) in the parental control cells without GFP-PCBP1 transfection (not green), while the red arrows point LC3B puncta in GFP-PCBP1-transfected cells (green). Bars equal to 25 μm. (C) Quantifications of LC3B puncta intensity per cell in B are presented as histograms (mean ± SD). Parent group indicates the parent control cells without GFP-PCBP1 (not green), while the PCBP1 group indicates the cells with transfected GFP-PCBP1 (green). ** P < 0.01; *** P < 0.001, n = 5. (D) Immunoblots of LC3B I, II in A2780 and DLD-1 cells with PCBP1 and GFP overexpression. Upon CQ or DMSO (control) treatment for 24 h, cells were analyzed. Immunoblot intensity ratio of LC3B II to GAPDH were, respectively, quantified and normalized, and indicated in each lane. (E) Immunofluorescence staining of LC3B puncta in both A2780 and DLD-1 cells with or without CQ treatment for 24 h. PCBP1 knockdown (KD) cells are in green, while parent control cells are not green. Cells counterstained with DAPI are in blue. White arrows point LC3B puncta (Red) in the PCBP1 KD cells, while the red arrows point LC3B puncta in the parental control cells. Scale bars in (B,E) equal to 25 μm.

    Techniques Used: Over Expression, Western Blot, Immunofluorescence, Staining, Transfection

    PCBP1 inhibits autophagy completion. (A) Immunoblots of p62 and GAPDH in the PCBP1 overexpression (GFP-PCBP1) and the GFP control cells by at least two independents. (B) Statistical analysis of p62 expression in PCBP1 overexpressing cells, compared with the GFP control cells by at least three independent immunoblots. ∗∗ p < 0.01. (C) Western blots of p62 in the indicated endogenous PCBP1 knockdown cells. Four GFP-confused shRNAs against PCBP1 were transfected into cells to establish the PCBP1 knockdown cells, while the GFP empty vector-transfected cells are control cells. (D) Immunoblots of p62 in A2780 and DLD-1 cells with PCBP1 and GFP overexpression. Upon CQ or DMSO (control) treatment for 24 h, cells were analyzed by at least two independents. (E) Immunoblots of p62 in A2780 and HCT-116 cells with PCBP1 knock down (KD) by at least two independents. GAPDH is used as an internal loading control, and the expression ratio of p62 to GAPDH was quantified and normalized, and indicated under each lane.
    Figure Legend Snippet: PCBP1 inhibits autophagy completion. (A) Immunoblots of p62 and GAPDH in the PCBP1 overexpression (GFP-PCBP1) and the GFP control cells by at least two independents. (B) Statistical analysis of p62 expression in PCBP1 overexpressing cells, compared with the GFP control cells by at least three independent immunoblots. ∗∗ p < 0.01. (C) Western blots of p62 in the indicated endogenous PCBP1 knockdown cells. Four GFP-confused shRNAs against PCBP1 were transfected into cells to establish the PCBP1 knockdown cells, while the GFP empty vector-transfected cells are control cells. (D) Immunoblots of p62 in A2780 and DLD-1 cells with PCBP1 and GFP overexpression. Upon CQ or DMSO (control) treatment for 24 h, cells were analyzed by at least two independents. (E) Immunoblots of p62 in A2780 and HCT-116 cells with PCBP1 knock down (KD) by at least two independents. GAPDH is used as an internal loading control, and the expression ratio of p62 to GAPDH was quantified and normalized, and indicated under each lane.

    Techniques Used: Western Blot, Over Expression, Expressing, Transfection, Plasmid Preparation

    PCBP1 enhance p62 expression in multiple levels. (A) Immunoblots of p62 and LC3B in the indicated GFP-PCBP1 cells as well as their parental cells treated without (Control) or with Actinomycin D (ActD) or MG132, respectively. (B) Semi-quantitative RT-PCR analysis of p62 mRNA stability (upper panel) in A2780 cells with endogenous PCBP1 knockdown (KD) or PCBP1 overexpression (PCBP1), compared with control cells (GFP) by at three independents. GAPDH is used as an internal control, and the ratio of p62 mRNA level to GAPDH was quantified, normalized and indicated under each lane. * P < 0.05. (C) Immunoblot of p62 protein level in DLD-1 cells with or without ATG5 knockdown by at least two independents. GAPDH was used as an internal loading control.
    Figure Legend Snippet: PCBP1 enhance p62 expression in multiple levels. (A) Immunoblots of p62 and LC3B in the indicated GFP-PCBP1 cells as well as their parental cells treated without (Control) or with Actinomycin D (ActD) or MG132, respectively. (B) Semi-quantitative RT-PCR analysis of p62 mRNA stability (upper panel) in A2780 cells with endogenous PCBP1 knockdown (KD) or PCBP1 overexpression (PCBP1), compared with control cells (GFP) by at three independents. GAPDH is used as an internal control, and the ratio of p62 mRNA level to GAPDH was quantified, normalized and indicated under each lane. * P < 0.05. (C) Immunoblot of p62 protein level in DLD-1 cells with or without ATG5 knockdown by at least two independents. GAPDH was used as an internal loading control.

    Techniques Used: Expressing, Western Blot, Quantitative RT-PCR, Over Expression

    PCBP1 overexpression enhances caspases activation for apoptosis. (A) Immunoblots of p62, PARP and caspases and their cleaved forms in A2780 and DLD-1 cells with PCBP1 and GFP overexpression at least two independents. (B) Immunoblots of p62, PARP and caspases and their cleaved forms in A2780 and HCT-116 cells with endogenous PCBP1 knockdown (KD), compared with A2780 and HCT-116 GFP controls by at least two independents. (C) Upon CQ treatments for 24 h, immunoblots of PARP, caspases and their cleaved forms in A2780 and DLD-1 cells with PCBP1 and GFP overexpression at least two independents. Arrows point and show the molecular weight of each protein. The cleaved forms of these proteins are shown as c-protein. (D) Flow cytometric analyses of the percentages of apoptotic cells in A2780 cells with PCBP1 overexpression, compared with the A2780 GFP control cells by at least two independents. Overall percentages of apoptotic cells are defined as the sum of Annexin-V positive cells.
    Figure Legend Snippet: PCBP1 overexpression enhances caspases activation for apoptosis. (A) Immunoblots of p62, PARP and caspases and their cleaved forms in A2780 and DLD-1 cells with PCBP1 and GFP overexpression at least two independents. (B) Immunoblots of p62, PARP and caspases and their cleaved forms in A2780 and HCT-116 cells with endogenous PCBP1 knockdown (KD), compared with A2780 and HCT-116 GFP controls by at least two independents. (C) Upon CQ treatments for 24 h, immunoblots of PARP, caspases and their cleaved forms in A2780 and DLD-1 cells with PCBP1 and GFP overexpression at least two independents. Arrows point and show the molecular weight of each protein. The cleaved forms of these proteins are shown as c-protein. (D) Flow cytometric analyses of the percentages of apoptotic cells in A2780 cells with PCBP1 overexpression, compared with the A2780 GFP control cells by at least two independents. Overall percentages of apoptotic cells are defined as the sum of Annexin-V positive cells.

    Techniques Used: Over Expression, Activation Assay, Western Blot, Molecular Weight

    colorectal cancer cell lines dld 1  (ATCC)


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    ATCC colorectal cancer cell lines dld 1
    Counts of colorectal cancer cells <t>(DLD-1,</t> HCT-116, HT-29) captured by a IsoFlux system and b the N50/S25/A25 fibrous mats (1 × 1 cm 2 ) with anti-EpCAM grafts, plotted with respect to the counts of cells loaded in 7-mL blood specimens
    Colorectal Cancer Cell Lines Dld 1, supplied by ATCC, 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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    1) Product Images from "Binary-blend fibber-based capture assay of circulating tumor cells for clinical diagnosis of colorectal cancer"

    Article Title: Binary-blend fibber-based capture assay of circulating tumor cells for clinical diagnosis of colorectal cancer

    Journal: Journal of Nanobiotechnology

    doi: 10.1186/s12951-017-0330-1

    Counts of colorectal cancer cells (DLD-1, HCT-116, HT-29) captured by a IsoFlux system and b the N50/S25/A25 fibrous mats (1 × 1 cm 2 ) with anti-EpCAM grafts, plotted with respect to the counts of cells loaded in 7-mL blood specimens
    Figure Legend Snippet: Counts of colorectal cancer cells (DLD-1, HCT-116, HT-29) captured by a IsoFlux system and b the N50/S25/A25 fibrous mats (1 × 1 cm 2 ) with anti-EpCAM grafts, plotted with respect to the counts of cells loaded in 7-mL blood specimens

    Techniques Used:

    SEM images of captured colorectal cancer cells: a DLD-1, b HCT-116, and c HT-29 on the N50/P50 fibrous mats, and d DLD-1 on a glass surface with anti-EpCAM grafts
    Figure Legend Snippet: SEM images of captured colorectal cancer cells: a DLD-1, b HCT-116, and c HT-29 on the N50/P50 fibrous mats, and d DLD-1 on a glass surface with anti-EpCAM grafts

    Techniques Used:

    human colorectal cancer cell lines dld 1  (ATCC)


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    human colorectal cancer cell lines dld 1  (ATCC)


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    human colorectal cancer cell lines dld 1  (ATCC)


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    human colorectal cancer cell lines dld 1  (ATCC)


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    ATCC human colorectal cancer cell lines dld 1
    Intestinal Dot1l affects the Wnt/β-catenin pathway. (a) Wnt/β-catenin downstream genes mRNA expression from Dot1l FF and Dot1l ΔIEC mice day 70 of the colorectal cancer model, n = 7–8, ** P = .0069 for Axin2 , **** P < .0001 for Sox4 , ** P = .0038 for Lgr5 , *** P = .0006 for Ephb3 , Student’s t-test. (b) Western blot of Axin2 expression from Dot1l FF and Dot1l ΔIEC mice day 70 of the colorectal cancer model. One of three is shown. (c) Immunofluorescence staining of β-catenin and Axin2 in Dot1l FF and Dot1l ΔIEC colorectal on day 14 of AOM-DSS model. Green: β-catenin, Red: Axin2, Blue: DAPI. (d and e) Effect of EPZ004777 on Wnt/β-catenin downstream gene mRNA expression in <t>DLD-1</t> (d) and HT29 (e) cells. (d) ** P = .0023 for AXIN2 , ** P = .0026 for SOX4 , * P = .0475 for EPHB3 , ** P = .0026 for LGR5 . (e) ** P = .0081 for AXIN2 , ** P = .0046 for SOX4 , ** P = .007 for EPHB3 . Student’s t-test. (f and g) Effect of DOT1L knockdown on Wnt/β-catenin downstream gene mRNA expression in DLD-1 (f) and HT29 (g) cells. (f) * P < .05 . (g) ** P = .0081 for AXIN2 , ** P = .0046 for SOX4 , ** P = .007 for EPHB3 , Student’s t-test. (h and i) H3K79me2 ChIP on the promoter (p) and different gene body regions (B1, B2, and B3) of SOX4 (h) and AXIN2 (i) in DLD-1 cells. NS, P > .05, * P ≤ .05, ** P ≤ .01, *** P ≤ .001, **** P ≤ .0001 , one-way ANOVA.
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    Intestinal Dot1l affects the Wnt/β-catenin pathway. (a) Wnt/β-catenin downstream genes mRNA expression from Dot1l FF and Dot1l ΔIEC mice day 70 of the colorectal cancer model, n = 7–8, ** P = .0069 for Axin2 , **** P < .0001 for Sox4 , ** P = .0038 for Lgr5 , *** P = .0006 for Ephb3 , Student’s t-test. (b) Western blot of Axin2 expression from Dot1l FF and Dot1l ΔIEC mice day 70 of the colorectal cancer model. One of three is shown. (c) Immunofluorescence staining of β-catenin and Axin2 in Dot1l FF and Dot1l ΔIEC colorectal on day 14 of AOM-DSS model. Green: β-catenin, Red: Axin2, Blue: DAPI. (d and e) Effect of EPZ004777 on Wnt/β-catenin downstream gene mRNA expression in DLD-1 (d) and HT29 (e) cells. (d) ** P = .0023 for AXIN2 , ** P = .0026 for SOX4 , * P = .0475 for EPHB3 , ** P = .0026 for LGR5 . (e) ** P = .0081 for AXIN2 , ** P = .0046 for SOX4 , ** P = .007 for EPHB3 . Student’s t-test. (f and g) Effect of DOT1L knockdown on Wnt/β-catenin downstream gene mRNA expression in DLD-1 (f) and HT29 (g) cells. (f) * P < .05 . (g) ** P = .0081 for AXIN2 , ** P = .0046 for SOX4 , ** P = .007 for EPHB3 , Student’s t-test. (h and i) H3K79me2 ChIP on the promoter (p) and different gene body regions (B1, B2, and B3) of SOX4 (h) and AXIN2 (i) in DLD-1 cells. NS, P > .05, * P ≤ .05, ** P ≤ .01, *** P ≤ .001, **** P ≤ .0001 , one-way ANOVA.

    Journal: Oncoimmunology

    Article Title: DOT1L affects colorectal carcinogenesis via altering T cell subsets and oncogenic pathway

    doi: 10.1080/2162402X.2022.2052640

    Figure Lengend Snippet: Intestinal Dot1l affects the Wnt/β-catenin pathway. (a) Wnt/β-catenin downstream genes mRNA expression from Dot1l FF and Dot1l ΔIEC mice day 70 of the colorectal cancer model, n = 7–8, ** P = .0069 for Axin2 , **** P < .0001 for Sox4 , ** P = .0038 for Lgr5 , *** P = .0006 for Ephb3 , Student’s t-test. (b) Western blot of Axin2 expression from Dot1l FF and Dot1l ΔIEC mice day 70 of the colorectal cancer model. One of three is shown. (c) Immunofluorescence staining of β-catenin and Axin2 in Dot1l FF and Dot1l ΔIEC colorectal on day 14 of AOM-DSS model. Green: β-catenin, Red: Axin2, Blue: DAPI. (d and e) Effect of EPZ004777 on Wnt/β-catenin downstream gene mRNA expression in DLD-1 (d) and HT29 (e) cells. (d) ** P = .0023 for AXIN2 , ** P = .0026 for SOX4 , * P = .0475 for EPHB3 , ** P = .0026 for LGR5 . (e) ** P = .0081 for AXIN2 , ** P = .0046 for SOX4 , ** P = .007 for EPHB3 . Student’s t-test. (f and g) Effect of DOT1L knockdown on Wnt/β-catenin downstream gene mRNA expression in DLD-1 (f) and HT29 (g) cells. (f) * P < .05 . (g) ** P = .0081 for AXIN2 , ** P = .0046 for SOX4 , ** P = .007 for EPHB3 , Student’s t-test. (h and i) H3K79me2 ChIP on the promoter (p) and different gene body regions (B1, B2, and B3) of SOX4 (h) and AXIN2 (i) in DLD-1 cells. NS, P > .05, * P ≤ .05, ** P ≤ .01, *** P ≤ .001, **** P ≤ .0001 , one-way ANOVA.

    Article Snippet: Human colorectal cancer cell lines DLD-1 and HT29 were obtained from ATCC.

    Techniques: Expressing, Western Blot, Immunofluorescence, Staining