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human bladder cancer cell lines j82  (DSMZ)


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    DSMZ human bladder cancer cell lines j82
    Homologous recombination (HR) deficiency confers cisplatin and PARP inhibitor sensitivity in bladder cancer cells. (a) Immunoblot showing siRNA-mediated depletion of BRCA2 protein in KU19-19 and <t>J82</t> bladder cancer cell lines. Vinculin is shown as a loading control. (b) Immunofluorescence (IF) microscopy shows loss of radiation-induced Rad51 foci formation in BRCA2-depleted compared to BRCA2-intact bladder cancer cells. (c) Cell viability assays demonstrate increased sensitivity to cisplatin following BRCA2 depletion in bladder cancer cell lines. (d) Cell viability assays demonstrate increased sensitivity to PARP inhibitors olaparib and talazoparib in bladder cancer cell lines. kDa, kilodalton. NTC, non-targeting control. Gy, Gray. MFI, mean fluorescence intensity. *p < 0.01 (IC50 values). Error bars represent standard deviation of data collected from assays performed in triplicate (panel B) or quadruplicate (panels C, D).
    Human Bladder Cancer Cell Lines J82, supplied by DSMZ, used in various techniques. Bioz Stars score: 94/100, based on 23 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+bladder+cancer+cell+lines+j82/KU-19-19/pmc11864231-35-0-13
    Average 94 stars, based on 23 article reviews
    human bladder cancer cell lines j82 - by Bioz Stars, 2026-10
    94/100 stars

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    1) Product Images from "Impact of DNA repair deficiency on sensitivity to antibody-drug conjugate (ADC) payloads in bladder cancer * "

    Article Title: Impact of DNA repair deficiency on sensitivity to antibody-drug conjugate (ADC) payloads in bladder cancer *

    Journal: Bladder Cancer

    doi: 10.1177/23523735251317865

    Homologous recombination (HR) deficiency confers cisplatin and PARP inhibitor sensitivity in bladder cancer cells. (a) Immunoblot showing siRNA-mediated depletion of BRCA2 protein in KU19-19 and J82 bladder cancer cell lines. Vinculin is shown as a loading control. (b) Immunofluorescence (IF) microscopy shows loss of radiation-induced Rad51 foci formation in BRCA2-depleted compared to BRCA2-intact bladder cancer cells. (c) Cell viability assays demonstrate increased sensitivity to cisplatin following BRCA2 depletion in bladder cancer cell lines. (d) Cell viability assays demonstrate increased sensitivity to PARP inhibitors olaparib and talazoparib in bladder cancer cell lines. kDa, kilodalton. NTC, non-targeting control. Gy, Gray. MFI, mean fluorescence intensity. *p < 0.01 (IC50 values). Error bars represent standard deviation of data collected from assays performed in triplicate (panel B) or quadruplicate (panels C, D).
    Figure Legend Snippet: Homologous recombination (HR) deficiency confers cisplatin and PARP inhibitor sensitivity in bladder cancer cells. (a) Immunoblot showing siRNA-mediated depletion of BRCA2 protein in KU19-19 and J82 bladder cancer cell lines. Vinculin is shown as a loading control. (b) Immunofluorescence (IF) microscopy shows loss of radiation-induced Rad51 foci formation in BRCA2-depleted compared to BRCA2-intact bladder cancer cells. (c) Cell viability assays demonstrate increased sensitivity to cisplatin following BRCA2 depletion in bladder cancer cell lines. (d) Cell viability assays demonstrate increased sensitivity to PARP inhibitors olaparib and talazoparib in bladder cancer cell lines. kDa, kilodalton. NTC, non-targeting control. Gy, Gray. MFI, mean fluorescence intensity. *p < 0.01 (IC50 values). Error bars represent standard deviation of data collected from assays performed in triplicate (panel B) or quadruplicate (panels C, D).

    Techniques Used: Homologous Recombination, Western Blot, Control, Immunofluorescence, Microscopy, Fluorescence, Standard Deviation

    Combined activity of MMAE and SN-38 with DNA repair inhibitors. (a) Cytotoxic activity of combining MMAE or SN-38 with ATR inhibition (berzosertib, BERZ), USP1 inhibition (ML323), or PARP inhibition (Olaparib, OLA; talazoparib, TALA) in KU19-19 (top graph) and J82 (bottom graph) bladder cancer cell lines with versus without HR deficiency conferred by BRCA2 depletion. (b) Cytotoxic activity of combining MMAE or SN-38 with ATR inhibition (berzosertib, BERZ), USP1 inhibition (ML323), or PARP inhibition (Olaparib, OLA; talazoparib, TALA) in NER-proficient ( ERCC2 WT) KU19-19 cells versus NER-deficient ( ERCC2 -mutant) KE182 cells (top graph) or NER-proficient (ERCC4 WT) H460 cells versus NER-deficient (ERCC4-deleted) H460 cells (bottom graph). Combination activity is quantified by the combination index (CI, see Methods) with positive log10(CI) values indicative of antagonism and negative log10(CI) values indicative of synergism. HRP, homologous recombination proficient (WT BRCA2); HRD, homologous recombination deficient (BRCA2 depleted); NERP, nucleotide excision repair proficient; NERD, nucleotide excision repair deficient. Error bars represent standard deviation of data collected from assays performed in quadruplicate.
    Figure Legend Snippet: Combined activity of MMAE and SN-38 with DNA repair inhibitors. (a) Cytotoxic activity of combining MMAE or SN-38 with ATR inhibition (berzosertib, BERZ), USP1 inhibition (ML323), or PARP inhibition (Olaparib, OLA; talazoparib, TALA) in KU19-19 (top graph) and J82 (bottom graph) bladder cancer cell lines with versus without HR deficiency conferred by BRCA2 depletion. (b) Cytotoxic activity of combining MMAE or SN-38 with ATR inhibition (berzosertib, BERZ), USP1 inhibition (ML323), or PARP inhibition (Olaparib, OLA; talazoparib, TALA) in NER-proficient ( ERCC2 WT) KU19-19 cells versus NER-deficient ( ERCC2 -mutant) KE182 cells (top graph) or NER-proficient (ERCC4 WT) H460 cells versus NER-deficient (ERCC4-deleted) H460 cells (bottom graph). Combination activity is quantified by the combination index (CI, see Methods) with positive log10(CI) values indicative of antagonism and negative log10(CI) values indicative of synergism. HRP, homologous recombination proficient (WT BRCA2); HRD, homologous recombination deficient (BRCA2 depleted); NERP, nucleotide excision repair proficient; NERD, nucleotide excision repair deficient. Error bars represent standard deviation of data collected from assays performed in quadruplicate.

    Techniques Used: Activity Assay, Inhibition, Mutagenesis, Homologous Recombination, Standard Deviation

    Related Articles

    Homologous Recombination:

    Article Title: Impact of DNA repair deficiency on sensitivity to antibody-drug conjugate (ADC) payloads in bladder cancer
    Article Snippet: Human bladder cancer cell lines J82 and KU19-19 were purchased from ATCC and DSMZ, respectively.. KE-182 is an ERCC2 -mutant derivative of KU19-19 created by CRISPR/Cas9-mediated gene editing.KE-182 is an ERCC2 -mutant derivative of KU19-19 created by CRISPR/Cas9-mediated gene editing.

    Article Title: Impact of DNA repair deficiency on sensitivity to antibody-drug conjugate (ADC) payloads in bladder cancer
    Article Snippet: Human bladder cancer cell lines J82 and KU19-19 were purchased from ATCC and DSMZ, respectively.. KE-182 is an ERCC2-mutant derivative of KU19-19 created by CRISPR/ Cas9-mediated gene editing.6 TheH460 human lung adenocarcinoma cell line with ERCC4 knockout has also been previously described.23 The CAPAN-1 (BRCA2-mutant) and CAPAN-1-CR (CAPAN-1cellswith stable expressionofwildtype BRCA2) human pancreatic adenocarcinoma cell lines were kind gifts from the Chris Lord laboratory.KE-182 is an ERCC2-mutant derivative of KU19-19 created by CRISPR/ Cas9-mediated gene editing.6 TheH460 human lung adenocarcinoma cell line with ERCC4 knockout has also been previously described.23 The CAPAN-1 (BRCA2-mutant) and CAPAN-1-CR (CAPAN-1cellswith stable expressionofwildtype BRCA2) human pancreatic adenocarcinoma cell lines were kind gifts from the Chris Lord laboratory.

    Western Blot:

    Article Title: Impact of DNA repair deficiency on sensitivity to antibody-drug conjugate (ADC) payloads in bladder cancer
    Article Snippet: Human bladder cancer cell lines J82 and KU19-19 were purchased from ATCC and DSMZ, respectively.. KE-182 is an ERCC2 -mutant derivative of KU19-19 created by CRISPR/Cas9-mediated gene editing.KE-182 is an ERCC2 -mutant derivative of KU19-19 created by CRISPR/Cas9-mediated gene editing.

    Article Title: Impact of DNA repair deficiency on sensitivity to antibody-drug conjugate (ADC) payloads in bladder cancer
    Article Snippet: Human bladder cancer cell lines J82 and KU19-19 were purchased from ATCC and DSMZ, respectively.. KE-182 is an ERCC2-mutant derivative of KU19-19 created by CRISPR/ Cas9-mediated gene editing.6 TheH460 human lung adenocarcinoma cell line with ERCC4 knockout has also been previously described.23 The CAPAN-1 (BRCA2-mutant) and CAPAN-1-CR (CAPAN-1cellswith stable expressionofwildtype BRCA2) human pancreatic adenocarcinoma cell lines were kind gifts from the Chris Lord laboratory.KE-182 is an ERCC2-mutant derivative of KU19-19 created by CRISPR/ Cas9-mediated gene editing.6 TheH460 human lung adenocarcinoma cell line with ERCC4 knockout has also been previously described.23 The CAPAN-1 (BRCA2-mutant) and CAPAN-1-CR (CAPAN-1cellswith stable expressionofwildtype BRCA2) human pancreatic adenocarcinoma cell lines were kind gifts from the Chris Lord laboratory.

    Control:

    Article Title: Impact of DNA repair deficiency on sensitivity to antibody-drug conjugate (ADC) payloads in bladder cancer
    Article Snippet: Human bladder cancer cell lines J82 and KU19-19 were purchased from ATCC and DSMZ, respectively.. KE-182 is an ERCC2 -mutant derivative of KU19-19 created by CRISPR/Cas9-mediated gene editing.KE-182 is an ERCC2 -mutant derivative of KU19-19 created by CRISPR/Cas9-mediated gene editing.

    Article Title: Impact of DNA repair deficiency on sensitivity to antibody-drug conjugate (ADC) payloads in bladder cancer
    Article Snippet: Human bladder cancer cell lines J82 and KU19-19 were purchased from ATCC and DSMZ, respectively.. KE-182 is an ERCC2-mutant derivative of KU19-19 created by CRISPR/ Cas9-mediated gene editing.6 TheH460 human lung adenocarcinoma cell line with ERCC4 knockout has also been previously described.23 The CAPAN-1 (BRCA2-mutant) and CAPAN-1-CR (CAPAN-1cellswith stable expressionofwildtype BRCA2) human pancreatic adenocarcinoma cell lines were kind gifts from the Chris Lord laboratory.KE-182 is an ERCC2-mutant derivative of KU19-19 created by CRISPR/ Cas9-mediated gene editing.6 TheH460 human lung adenocarcinoma cell line with ERCC4 knockout has also been previously described.23 The CAPAN-1 (BRCA2-mutant) and CAPAN-1-CR (CAPAN-1cellswith stable expressionofwildtype BRCA2) human pancreatic adenocarcinoma cell lines were kind gifts from the Chris Lord laboratory.

    Immunofluorescence:

    Article Title: Impact of DNA repair deficiency on sensitivity to antibody-drug conjugate (ADC) payloads in bladder cancer
    Article Snippet: Human bladder cancer cell lines J82 and KU19-19 were purchased from ATCC and DSMZ, respectively.. KE-182 is an ERCC2 -mutant derivative of KU19-19 created by CRISPR/Cas9-mediated gene editing.KE-182 is an ERCC2 -mutant derivative of KU19-19 created by CRISPR/Cas9-mediated gene editing.

    Article Title: Impact of DNA repair deficiency on sensitivity to antibody-drug conjugate (ADC) payloads in bladder cancer
    Article Snippet: Human bladder cancer cell lines J82 and KU19-19 were purchased from ATCC and DSMZ, respectively.. KE-182 is an ERCC2-mutant derivative of KU19-19 created by CRISPR/ Cas9-mediated gene editing.6 TheH460 human lung adenocarcinoma cell line with ERCC4 knockout has also been previously described.23 The CAPAN-1 (BRCA2-mutant) and CAPAN-1-CR (CAPAN-1cellswith stable expressionofwildtype BRCA2) human pancreatic adenocarcinoma cell lines were kind gifts from the Chris Lord laboratory.KE-182 is an ERCC2-mutant derivative of KU19-19 created by CRISPR/ Cas9-mediated gene editing.6 TheH460 human lung adenocarcinoma cell line with ERCC4 knockout has also been previously described.23 The CAPAN-1 (BRCA2-mutant) and CAPAN-1-CR (CAPAN-1cellswith stable expressionofwildtype BRCA2) human pancreatic adenocarcinoma cell lines were kind gifts from the Chris Lord laboratory.

    Microscopy:

    Article Title: Impact of DNA repair deficiency on sensitivity to antibody-drug conjugate (ADC) payloads in bladder cancer
    Article Snippet: Human bladder cancer cell lines J82 and KU19-19 were purchased from ATCC and DSMZ, respectively.. KE-182 is an ERCC2 -mutant derivative of KU19-19 created by CRISPR/Cas9-mediated gene editing.KE-182 is an ERCC2 -mutant derivative of KU19-19 created by CRISPR/Cas9-mediated gene editing.

    Article Title: Impact of DNA repair deficiency on sensitivity to antibody-drug conjugate (ADC) payloads in bladder cancer
    Article Snippet: Human bladder cancer cell lines J82 and KU19-19 were purchased from ATCC and DSMZ, respectively.. KE-182 is an ERCC2-mutant derivative of KU19-19 created by CRISPR/ Cas9-mediated gene editing.6 TheH460 human lung adenocarcinoma cell line with ERCC4 knockout has also been previously described.23 The CAPAN-1 (BRCA2-mutant) and CAPAN-1-CR (CAPAN-1cellswith stable expressionofwildtype BRCA2) human pancreatic adenocarcinoma cell lines were kind gifts from the Chris Lord laboratory.KE-182 is an ERCC2-mutant derivative of KU19-19 created by CRISPR/ Cas9-mediated gene editing.6 TheH460 human lung adenocarcinoma cell line with ERCC4 knockout has also been previously described.23 The CAPAN-1 (BRCA2-mutant) and CAPAN-1-CR (CAPAN-1cellswith stable expressionofwildtype BRCA2) human pancreatic adenocarcinoma cell lines were kind gifts from the Chris Lord laboratory.

    Fluorescence:

    Article Title: Impact of DNA repair deficiency on sensitivity to antibody-drug conjugate (ADC) payloads in bladder cancer
    Article Snippet: Human bladder cancer cell lines J82 and KU19-19 were purchased from ATCC and DSMZ, respectively.. KE-182 is an ERCC2 -mutant derivative of KU19-19 created by CRISPR/Cas9-mediated gene editing.KE-182 is an ERCC2 -mutant derivative of KU19-19 created by CRISPR/Cas9-mediated gene editing.

    Article Title: Impact of DNA repair deficiency on sensitivity to antibody-drug conjugate (ADC) payloads in bladder cancer
    Article Snippet: Human bladder cancer cell lines J82 and KU19-19 were purchased from ATCC and DSMZ, respectively.. KE-182 is an ERCC2-mutant derivative of KU19-19 created by CRISPR/ Cas9-mediated gene editing.6 TheH460 human lung adenocarcinoma cell line with ERCC4 knockout has also been previously described.23 The CAPAN-1 (BRCA2-mutant) and CAPAN-1-CR (CAPAN-1cellswith stable expressionofwildtype BRCA2) human pancreatic adenocarcinoma cell lines were kind gifts from the Chris Lord laboratory.KE-182 is an ERCC2-mutant derivative of KU19-19 created by CRISPR/ Cas9-mediated gene editing.6 TheH460 human lung adenocarcinoma cell line with ERCC4 knockout has also been previously described.23 The CAPAN-1 (BRCA2-mutant) and CAPAN-1-CR (CAPAN-1cellswith stable expressionofwildtype BRCA2) human pancreatic adenocarcinoma cell lines were kind gifts from the Chris Lord laboratory.

    Standard Deviation:

    Article Title: Impact of DNA repair deficiency on sensitivity to antibody-drug conjugate (ADC) payloads in bladder cancer
    Article Snippet: Human bladder cancer cell lines J82 and KU19-19 were purchased from ATCC and DSMZ, respectively.. KE-182 is an ERCC2 -mutant derivative of KU19-19 created by CRISPR/Cas9-mediated gene editing.KE-182 is an ERCC2 -mutant derivative of KU19-19 created by CRISPR/Cas9-mediated gene editing.

    Article Title: Impact of DNA repair deficiency on sensitivity to antibody-drug conjugate (ADC) payloads in bladder cancer
    Article Snippet: Human bladder cancer cell lines J82 and KU19-19 were purchased from ATCC and DSMZ, respectively.. KE-182 is an ERCC2-mutant derivative of KU19-19 created by CRISPR/ Cas9-mediated gene editing.6 TheH460 human lung adenocarcinoma cell line with ERCC4 knockout has also been previously described.23 The CAPAN-1 (BRCA2-mutant) and CAPAN-1-CR (CAPAN-1cellswith stable expressionofwildtype BRCA2) human pancreatic adenocarcinoma cell lines were kind gifts from the Chris Lord laboratory.KE-182 is an ERCC2-mutant derivative of KU19-19 created by CRISPR/ Cas9-mediated gene editing.6 TheH460 human lung adenocarcinoma cell line with ERCC4 knockout has also been previously described.23 The CAPAN-1 (BRCA2-mutant) and CAPAN-1-CR (CAPAN-1cellswith stable expressionofwildtype BRCA2) human pancreatic adenocarcinoma cell lines were kind gifts from the Chris Lord laboratory.

    Activity Assay:

    Article Title: Impact of DNA repair deficiency on sensitivity to antibody-drug conjugate (ADC) payloads in bladder cancer
    Article Snippet: Human bladder cancer cell lines J82 and KU19-19 were purchased from ATCC and DSMZ, respectively.. KE-182 is an ERCC2 -mutant derivative of KU19-19 created by CRISPR/Cas9-mediated gene editing.KE-182 is an ERCC2 -mutant derivative of KU19-19 created by CRISPR/Cas9-mediated gene editing.

    Article Title: Impact of DNA repair deficiency on sensitivity to antibody-drug conjugate (ADC) payloads in bladder cancer
    Article Snippet: Human bladder cancer cell lines J82 and KU19-19 were purchased from ATCC and DSMZ, respectively.. KE-182 is an ERCC2-mutant derivative of KU19-19 created by CRISPR/ Cas9-mediated gene editing.6 TheH460 human lung adenocarcinoma cell line with ERCC4 knockout has also been previously described.23 The CAPAN-1 (BRCA2-mutant) and CAPAN-1-CR (CAPAN-1cellswith stable expressionofwildtype BRCA2) human pancreatic adenocarcinoma cell lines were kind gifts from the Chris Lord laboratory.KE-182 is an ERCC2-mutant derivative of KU19-19 created by CRISPR/ Cas9-mediated gene editing.6 TheH460 human lung adenocarcinoma cell line with ERCC4 knockout has also been previously described.23 The CAPAN-1 (BRCA2-mutant) and CAPAN-1-CR (CAPAN-1cellswith stable expressionofwildtype BRCA2) human pancreatic adenocarcinoma cell lines were kind gifts from the Chris Lord laboratory.

    Inhibition:

    Article Title: Impact of DNA repair deficiency on sensitivity to antibody-drug conjugate (ADC) payloads in bladder cancer
    Article Snippet: Human bladder cancer cell lines J82 and KU19-19 were purchased from ATCC and DSMZ, respectively.. KE-182 is an ERCC2 -mutant derivative of KU19-19 created by CRISPR/Cas9-mediated gene editing.KE-182 is an ERCC2 -mutant derivative of KU19-19 created by CRISPR/Cas9-mediated gene editing.

    Article Title: Impact of DNA repair deficiency on sensitivity to antibody-drug conjugate (ADC) payloads in bladder cancer
    Article Snippet: Human bladder cancer cell lines J82 and KU19-19 were purchased from ATCC and DSMZ, respectively.. KE-182 is an ERCC2-mutant derivative of KU19-19 created by CRISPR/ Cas9-mediated gene editing.6 TheH460 human lung adenocarcinoma cell line with ERCC4 knockout has also been previously described.23 The CAPAN-1 (BRCA2-mutant) and CAPAN-1-CR (CAPAN-1cellswith stable expressionofwildtype BRCA2) human pancreatic adenocarcinoma cell lines were kind gifts from the Chris Lord laboratory.KE-182 is an ERCC2-mutant derivative of KU19-19 created by CRISPR/ Cas9-mediated gene editing.6 TheH460 human lung adenocarcinoma cell line with ERCC4 knockout has also been previously described.23 The CAPAN-1 (BRCA2-mutant) and CAPAN-1-CR (CAPAN-1cellswith stable expressionofwildtype BRCA2) human pancreatic adenocarcinoma cell lines were kind gifts from the Chris Lord laboratory.

    Mutagenesis:

    Article Title: Impact of DNA repair deficiency on sensitivity to antibody-drug conjugate (ADC) payloads in bladder cancer
    Article Snippet: Human bladder cancer cell lines J82 and KU19-19 were purchased from ATCC and DSMZ, respectively.. KE-182 is an ERCC2 -mutant derivative of KU19-19 created by CRISPR/Cas9-mediated gene editing.KE-182 is an ERCC2 -mutant derivative of KU19-19 created by CRISPR/Cas9-mediated gene editing.

    Article Title: Impact of DNA repair deficiency on sensitivity to antibody-drug conjugate (ADC) payloads in bladder cancer
    Article Snippet: Human bladder cancer cell lines J82 and KU19-19 were purchased from ATCC and DSMZ, respectively.. KE-182 is an ERCC2-mutant derivative of KU19-19 created by CRISPR/ Cas9-mediated gene editing.6 TheH460 human lung adenocarcinoma cell line with ERCC4 knockout has also been previously described.23 The CAPAN-1 (BRCA2-mutant) and CAPAN-1-CR (CAPAN-1cellswith stable expressionofwildtype BRCA2) human pancreatic adenocarcinoma cell lines were kind gifts from the Chris Lord laboratory.KE-182 is an ERCC2-mutant derivative of KU19-19 created by CRISPR/ Cas9-mediated gene editing.6 TheH460 human lung adenocarcinoma cell line with ERCC4 knockout has also been previously described.23 The CAPAN-1 (BRCA2-mutant) and CAPAN-1-CR (CAPAN-1cellswith stable expressionofwildtype BRCA2) human pancreatic adenocarcinoma cell lines were kind gifts from the Chris Lord laboratory.



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    (a) Representative Integrative Genomics Viewer (IGV) browser tracks showing baseline ATAC-seq chromatin accessibility near the transcription start sites of six MHC-II loci (CIITA, CD74, HLA-DRA, HLA-DRB1, HLA-DQB1, HLA-DPA1) in five bladder cancer <t>cell</t> <t>lines.</t> Within each gene panel, all tracks share a common y-axis scale (indicated in the upper-left corner); RefSeq gene annotations are shown at the bottom. Most cell lines display accessible chromatin at MHC-II promoters at baseline despite negligible transcriptional output, indicating an epigenetically poised state. <t>J82</t> and SW-780 are exceptions, showing minimal baseline accessibility. (b) IGV browser tracks showing ATAC-seq chromatin accessibility (blue) and RNA-seq signal (red) at MHC-II loci in J82 at baseline and following IFN-γ stimulation. IFN-γ induces de novo chromatin opening at the CIITA and HLA-DRA promoters accompanied by transcriptional activation, demonstrating that inflammatory signaling can actively remodel previously inaccessible MHC-II loci. Shared y-axis scales within each data type are indicated. (c) Heatmap of RNA-seq expression values (TPM) for MHC-II pathway genes across six bladder cancer cell lines (SCaBER, TCCSUP, RT4, 5637, SW-780, J82) at 0 hr and 72 hr (48 hr for RT4) following IFN-γ stimulation (10 ng/mL). Five of six lines show robust, coordinated MHC-II induction; SW-780 shows an attenuated transcriptional response. (d) Representative flow cytometry histograms showing surface MHC-II (HLA-DR) protein expression in six bladder cancer cell lines at baseline (gray/unfilled) and after 72 h IFN-γ stimulation at the indicated dose (colored/filled). Five of six lines display clear surface MHC-II upregulation. SW-780 is the sole non-responder at the protein level, consistent with the locus-specific chromatin barrier shown in Supplementary Figure 2f. (e) Gene set enrichment analysis (GSEA) testing the consensus in vitro IFN-γ response signature in patient tumor cells. The in vitro IFN-γ UP signature is enriched in MHC-II-high malignant epithelial cells, and the in vitro IFN-γ DOWN signature is enriched in MHC-II-low cells (internal snRNA-seq cohort). Gene sets are ranked by normalized enrichment score. (f) Genome-wide concordance between the in vitro and in vivo IFN-γ responses. Each point is a gene; axes show log₂ fold change in IFN-γ-stimulated versus unstimulated cell lines (median across five responsive lines) and in MHC-II-high versus MHC-II-low malignant cells in vivo (Spearman ρ = 0.27, p < 0.001). MHC-I and MHC-II antigen-presentation genes and interferon-responsive effector genes (CXCL10, CXCL11, IL32, ICAM1) are among the most concordant upregulated features; basal/squamous markers (KRT5, KRT13, ZNF750, IVL) are among the most concordant downregulated features.
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    Homologous recombination (HR) deficiency confers cisplatin and PARP inhibitor sensitivity in bladder cancer cells. (a) Immunoblot showing siRNA-mediated depletion of BRCA2 protein in KU19-19 and <t>J82</t> bladder cancer cell lines. Vinculin is shown as a loading control. (b) Immunofluorescence (IF) microscopy shows loss of radiation-induced Rad51 foci formation in BRCA2-depleted compared to BRCA2-intact bladder cancer cells. (c) Cell viability assays demonstrate increased sensitivity to cisplatin following BRCA2 depletion in bladder cancer cell lines. (d) Cell viability assays demonstrate increased sensitivity to PARP inhibitors olaparib and talazoparib in bladder cancer cell lines. kDa, kilodalton. NTC, non-targeting control. Gy, Gray. MFI, mean fluorescence intensity. *p < 0.01 (IC50 values). Error bars represent standard deviation of data collected from assays performed in triplicate (panel B) or quadruplicate (panels C, D).
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    (a) Representative Integrative Genomics Viewer (IGV) browser tracks showing baseline ATAC-seq chromatin accessibility near the transcription start sites of six MHC-II loci (CIITA, CD74, HLA-DRA, HLA-DRB1, HLA-DQB1, HLA-DPA1) in five bladder cancer cell lines. Within each gene panel, all tracks share a common y-axis scale (indicated in the upper-left corner); RefSeq gene annotations are shown at the bottom. Most cell lines display accessible chromatin at MHC-II promoters at baseline despite negligible transcriptional output, indicating an epigenetically poised state. J82 and SW-780 are exceptions, showing minimal baseline accessibility. (b) IGV browser tracks showing ATAC-seq chromatin accessibility (blue) and RNA-seq signal (red) at MHC-II loci in J82 at baseline and following IFN-γ stimulation. IFN-γ induces de novo chromatin opening at the CIITA and HLA-DRA promoters accompanied by transcriptional activation, demonstrating that inflammatory signaling can actively remodel previously inaccessible MHC-II loci. Shared y-axis scales within each data type are indicated. (c) Heatmap of RNA-seq expression values (TPM) for MHC-II pathway genes across six bladder cancer cell lines (SCaBER, TCCSUP, RT4, 5637, SW-780, J82) at 0 hr and 72 hr (48 hr for RT4) following IFN-γ stimulation (10 ng/mL). Five of six lines show robust, coordinated MHC-II induction; SW-780 shows an attenuated transcriptional response. (d) Representative flow cytometry histograms showing surface MHC-II (HLA-DR) protein expression in six bladder cancer cell lines at baseline (gray/unfilled) and after 72 h IFN-γ stimulation at the indicated dose (colored/filled). Five of six lines display clear surface MHC-II upregulation. SW-780 is the sole non-responder at the protein level, consistent with the locus-specific chromatin barrier shown in Supplementary Figure 2f. (e) Gene set enrichment analysis (GSEA) testing the consensus in vitro IFN-γ response signature in patient tumor cells. The in vitro IFN-γ UP signature is enriched in MHC-II-high malignant epithelial cells, and the in vitro IFN-γ DOWN signature is enriched in MHC-II-low cells (internal snRNA-seq cohort). Gene sets are ranked by normalized enrichment score. (f) Genome-wide concordance between the in vitro and in vivo IFN-γ responses. Each point is a gene; axes show log₂ fold change in IFN-γ-stimulated versus unstimulated cell lines (median across five responsive lines) and in MHC-II-high versus MHC-II-low malignant cells in vivo (Spearman ρ = 0.27, p < 0.001). MHC-I and MHC-II antigen-presentation genes and interferon-responsive effector genes (CXCL10, CXCL11, IL32, ICAM1) are among the most concordant upregulated features; basal/squamous markers (KRT5, KRT13, ZNF750, IVL) are among the most concordant downregulated features.

    Journal: bioRxiv

    Article Title: A tumor-cell MHC-II program is associated with checkpoint-blockade outcomes across stages of bladder cancer

    doi: 10.64898/2026.09.21.753036

    Figure Lengend Snippet: (a) Representative Integrative Genomics Viewer (IGV) browser tracks showing baseline ATAC-seq chromatin accessibility near the transcription start sites of six MHC-II loci (CIITA, CD74, HLA-DRA, HLA-DRB1, HLA-DQB1, HLA-DPA1) in five bladder cancer cell lines. Within each gene panel, all tracks share a common y-axis scale (indicated in the upper-left corner); RefSeq gene annotations are shown at the bottom. Most cell lines display accessible chromatin at MHC-II promoters at baseline despite negligible transcriptional output, indicating an epigenetically poised state. J82 and SW-780 are exceptions, showing minimal baseline accessibility. (b) IGV browser tracks showing ATAC-seq chromatin accessibility (blue) and RNA-seq signal (red) at MHC-II loci in J82 at baseline and following IFN-γ stimulation. IFN-γ induces de novo chromatin opening at the CIITA and HLA-DRA promoters accompanied by transcriptional activation, demonstrating that inflammatory signaling can actively remodel previously inaccessible MHC-II loci. Shared y-axis scales within each data type are indicated. (c) Heatmap of RNA-seq expression values (TPM) for MHC-II pathway genes across six bladder cancer cell lines (SCaBER, TCCSUP, RT4, 5637, SW-780, J82) at 0 hr and 72 hr (48 hr for RT4) following IFN-γ stimulation (10 ng/mL). Five of six lines show robust, coordinated MHC-II induction; SW-780 shows an attenuated transcriptional response. (d) Representative flow cytometry histograms showing surface MHC-II (HLA-DR) protein expression in six bladder cancer cell lines at baseline (gray/unfilled) and after 72 h IFN-γ stimulation at the indicated dose (colored/filled). Five of six lines display clear surface MHC-II upregulation. SW-780 is the sole non-responder at the protein level, consistent with the locus-specific chromatin barrier shown in Supplementary Figure 2f. (e) Gene set enrichment analysis (GSEA) testing the consensus in vitro IFN-γ response signature in patient tumor cells. The in vitro IFN-γ UP signature is enriched in MHC-II-high malignant epithelial cells, and the in vitro IFN-γ DOWN signature is enriched in MHC-II-low cells (internal snRNA-seq cohort). Gene sets are ranked by normalized enrichment score. (f) Genome-wide concordance between the in vitro and in vivo IFN-γ responses. Each point is a gene; axes show log₂ fold change in IFN-γ-stimulated versus unstimulated cell lines (median across five responsive lines) and in MHC-II-high versus MHC-II-low malignant cells in vivo (Spearman ρ = 0.27, p < 0.001). MHC-I and MHC-II antigen-presentation genes and interferon-responsive effector genes (CXCL10, CXCL11, IL32, ICAM1) are among the most concordant upregulated features; basal/squamous markers (KRT5, KRT13, ZNF750, IVL) are among the most concordant downregulated features.

    Article Snippet: The human bladder cancer cell lines J82 (HTB-1), TCCSUP (HTB-5), SCaBER (HTB-3), 5637 (HTB-9), RT4 (HTB-2), and SW780 (CRL-2169) were procured from ATCC and maintained under conditions recommended by ATCC.

    Techniques: RNA Sequencing, Activation Assay, Expressing, Flow Cytometry, Analysis, In Vitro, Genome Wide, In Vivo, Immunopeptidomics

    Homologous recombination (HR) deficiency confers cisplatin and PARP inhibitor sensitivity in bladder cancer cells. (a) Immunoblot showing siRNA-mediated depletion of BRCA2 protein in KU19-19 and J82 bladder cancer cell lines. Vinculin is shown as a loading control. (b) Immunofluorescence (IF) microscopy shows loss of radiation-induced Rad51 foci formation in BRCA2-depleted compared to BRCA2-intact bladder cancer cells. (c) Cell viability assays demonstrate increased sensitivity to cisplatin following BRCA2 depletion in bladder cancer cell lines. (d) Cell viability assays demonstrate increased sensitivity to PARP inhibitors olaparib and talazoparib in bladder cancer cell lines. kDa, kilodalton. NTC, non-targeting control. Gy, Gray. MFI, mean fluorescence intensity. *p < 0.01 (IC50 values). Error bars represent standard deviation of data collected from assays performed in triplicate (panel B) or quadruplicate (panels C, D).

    Journal: Bladder Cancer

    Article Title: Impact of DNA repair deficiency on sensitivity to antibody-drug conjugate (ADC) payloads in bladder cancer *

    doi: 10.1177/23523735251317865

    Figure Lengend Snippet: Homologous recombination (HR) deficiency confers cisplatin and PARP inhibitor sensitivity in bladder cancer cells. (a) Immunoblot showing siRNA-mediated depletion of BRCA2 protein in KU19-19 and J82 bladder cancer cell lines. Vinculin is shown as a loading control. (b) Immunofluorescence (IF) microscopy shows loss of radiation-induced Rad51 foci formation in BRCA2-depleted compared to BRCA2-intact bladder cancer cells. (c) Cell viability assays demonstrate increased sensitivity to cisplatin following BRCA2 depletion in bladder cancer cell lines. (d) Cell viability assays demonstrate increased sensitivity to PARP inhibitors olaparib and talazoparib in bladder cancer cell lines. kDa, kilodalton. NTC, non-targeting control. Gy, Gray. MFI, mean fluorescence intensity. *p < 0.01 (IC50 values). Error bars represent standard deviation of data collected from assays performed in triplicate (panel B) or quadruplicate (panels C, D).

    Article Snippet: Human bladder cancer cell lines J82 and KU19-19 were purchased from ATCC and DSMZ, respectively.

    Techniques: Homologous Recombination, Western Blot, Control, Immunofluorescence, Microscopy, Fluorescence, Standard Deviation

    Combined activity of MMAE and SN-38 with DNA repair inhibitors. (a) Cytotoxic activity of combining MMAE or SN-38 with ATR inhibition (berzosertib, BERZ), USP1 inhibition (ML323), or PARP inhibition (Olaparib, OLA; talazoparib, TALA) in KU19-19 (top graph) and J82 (bottom graph) bladder cancer cell lines with versus without HR deficiency conferred by BRCA2 depletion. (b) Cytotoxic activity of combining MMAE or SN-38 with ATR inhibition (berzosertib, BERZ), USP1 inhibition (ML323), or PARP inhibition (Olaparib, OLA; talazoparib, TALA) in NER-proficient ( ERCC2 WT) KU19-19 cells versus NER-deficient ( ERCC2 -mutant) KE182 cells (top graph) or NER-proficient (ERCC4 WT) H460 cells versus NER-deficient (ERCC4-deleted) H460 cells (bottom graph). Combination activity is quantified by the combination index (CI, see Methods) with positive log10(CI) values indicative of antagonism and negative log10(CI) values indicative of synergism. HRP, homologous recombination proficient (WT BRCA2); HRD, homologous recombination deficient (BRCA2 depleted); NERP, nucleotide excision repair proficient; NERD, nucleotide excision repair deficient. Error bars represent standard deviation of data collected from assays performed in quadruplicate.

    Journal: Bladder Cancer

    Article Title: Impact of DNA repair deficiency on sensitivity to antibody-drug conjugate (ADC) payloads in bladder cancer *

    doi: 10.1177/23523735251317865

    Figure Lengend Snippet: Combined activity of MMAE and SN-38 with DNA repair inhibitors. (a) Cytotoxic activity of combining MMAE or SN-38 with ATR inhibition (berzosertib, BERZ), USP1 inhibition (ML323), or PARP inhibition (Olaparib, OLA; talazoparib, TALA) in KU19-19 (top graph) and J82 (bottom graph) bladder cancer cell lines with versus without HR deficiency conferred by BRCA2 depletion. (b) Cytotoxic activity of combining MMAE or SN-38 with ATR inhibition (berzosertib, BERZ), USP1 inhibition (ML323), or PARP inhibition (Olaparib, OLA; talazoparib, TALA) in NER-proficient ( ERCC2 WT) KU19-19 cells versus NER-deficient ( ERCC2 -mutant) KE182 cells (top graph) or NER-proficient (ERCC4 WT) H460 cells versus NER-deficient (ERCC4-deleted) H460 cells (bottom graph). Combination activity is quantified by the combination index (CI, see Methods) with positive log10(CI) values indicative of antagonism and negative log10(CI) values indicative of synergism. HRP, homologous recombination proficient (WT BRCA2); HRD, homologous recombination deficient (BRCA2 depleted); NERP, nucleotide excision repair proficient; NERD, nucleotide excision repair deficient. Error bars represent standard deviation of data collected from assays performed in quadruplicate.

    Article Snippet: Human bladder cancer cell lines J82 and KU19-19 were purchased from ATCC and DSMZ, respectively.

    Techniques: Activity Assay, Inhibition, Mutagenesis, Homologous Recombination, Standard Deviation