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Differential Gene Expression between Chemoresistant and Chemosensitive T24 Human Bladder Cancer Cells

ABSTRACT: This project employed proteomics to analyze protein expression profiles between chemoresistant and chemosensitive variants of the human bladder cancer T24 cell line. The objective was to identify key differentially expressed proteins and their associated signaling pathways involved in chemotherapy resistance. The findings aim to provide new insights and potential therapeutic targets for overcoming chemoresistance in bladder cancer.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Urinary Bladder

SUBMITTER: Weiyang He

LAB HEAD: Weiyang He

PROVIDER: PXD069140 | Pride | 2026-02-09

REPOSITORIES: Pride

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			Action	DRS
	HFX7_FFRA23H0004.msf	Msf
	HFX7_FFRA23H0004.pdResult	Other
	HFX7_FFRA23H000411-1A.raw	Raw
	HFX7_FFRA23H000412-1A.raw	Raw
	HFX7_FFRA23H000413-1A.raw	Raw

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Publications

The FN1-ITGB4 Axis Drives Acquired Chemoresistance in Bladder Cancer by Activating FAK Signaling.

Zhang Xiaoyu X Zong RenFei R Sun Yan Y Chen Nan N Zhu Kunyao K Tong Hang H Li Tinghao T Zhu Junlong J Qin Zijia Z Wu Linfeng L Wang Aimin A He Weiyang W

Oncology research 20260119 2

<h4>Objective</h4>While cisplatin-based chemotherapy is pivotal for advanced bladder cancer, acquired resistance remains a major obstacle. This study investigates key molecular drivers of this resistance and potential reversal strategies.<h4>Methods</h4>We established GC (Gemcitabine and Cisplatin)-resistant T24-R and UC3-R cell lines from T24 and UM-UC-3 (UC3) cells. Transcriptomic and proteomic analyses identified differentially expressed molecules. Apoptosis and cell viability were assessed b ...[more]

PMID: 41613793

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Acquired semi-squamalization during chemotherapy suggests a differentiation therapy for bladder cancer

Project description:Cisplatin-based chemotherapy is the most common treatment for unresectable bladder cancers and also increasingly used as neoadjuvant treatments before or after surgery and radiotherapy. Unfortunately, though many patients respond to the treatment, most of them develop resistance quickly with unclear mechanisms and few further treatment options. Here, we report that semi-squamazation is acquired during chemo treatment in both mice and human. Multi-omics analyses show that cathepsin H (CTSH), a direct target of p63, is associated with chemoresistance and semi-squamation. Treatment with the cathepsin inhibitor E64 specifically restrains chemoresistant but not chemosensitive cancer. Mechanistically, cathepsin inhibition induces fully squamous differentiation of bladder cancer cells, which requires TNF receptor 1alpha and is associated with pyroptosis. Our study suggests that semi-squamazation would be a diagnosistic marker for chemoresistance and differentiation therapy by targeting CTSH might be a potential treatment for chemoresistant bladder cancer.

2022-07-09 | GSE192575 | GEO

Enzalutamide inhibits proliferation of gemcitabine-resistant bladder cancer cells with increased androgen receptor expression

Project description:Advanced bladder cancer is treated mainly with gemcitabine and cisplatin, but most patients eventually become resistance to these chemotherapeutic agents. Androgen receptor (AR) signaling has been implicated in bladder cancer as well as other types of cancer including prostate cancer. In the present study, we showed the expression and role of AR in gemcitabine-resistant bladder cancer cells and examined the potential of enzalutamide, an AR inhibitor, as a therapeutic for the chemoresistance. First of all, we established gemcitabine-resistant T24 cells (T24GR) from T24 bladder cancer cells and performed gene expression profiling and network analysis, which revealed increased AR expression and AR-related gene network in T24GR cells. Quantitative RT-PCR and Western blot analysis confirmed increased expression of AR in T24GR cells compared with parental T24 cells, which was associated with more potent transcriptional activity of AR in T24GR cells. The number of AR gene copy in T24GR cells was twice as many as that of T24 cells. Knockdown of AR expression by siRNA resulted in inhibition of proliferation of T24GR cells. Cell culture in charcoal-stripped serum and treatment with enzalutamide also inhibited growth of T24GR cells, which was accompanied by cell cycle arrest. Lastly, the AR transcriptional activity was found to be reduced in T24GR cells by enzalutamide treatment. Our results suggest that blockade of AR signaling by enzalutamide might be effective for patients with advanced gemcitabine-resistant bladder cancer with increased AR expression.

2016-11-30 | GSE77883 | GEO

Proteogenomic characterization of muscle invasive bladder cancer

Project description:To explore potential chemoresistance mechanisms and identify therapeutic opportunities in muscle invasive bladder cancer (MIBC), we conducted comprehensive proteogenomic characterization of 46 pre- and 14 post-treatment MIBC tumors incorporating genomics, transcriptomics, proteomics, and phosphoproteomics. Multi-omics clustering not only recapitulated established molecular subtypes, but also revealed subtypes associated with chemotherapy sensitivity. Protein isoform level analysis identified protein abundance of a short isoform of ATAD1 and RAF family proteins as biomarkers of chemosensitivity. Integration of proteomic and phosphoproteomic data revealed Wnt signaling via GSK3B-S9 phosphorylation and the JAK/STAT pathway as potential targets to overcome chemoresistance. Correlations between PD-L1 and TROP-2/NECTIN-4 indicate an additive benefit of combination therapy targeting these proteins. Overall, this study serves as a valuable resource for researchers and clinicians aiming to better understand and treat chemoresistant MIBC.

2025-09-22 | PXD060290 | Pride

Expression data for T24 bladder cancer cell line - scrambled, SOX4-KD and SOX4 overexpression

Project description:We knocked down SOX4 in T24 cell and created 3 cell lines: T24-scrambled, T24-SOX4-knockdown and T24-SOX4-rescue and compared gene expression changes SOX4 is a developmental transcription factor that is overexpressed in as many as 23% of bladder cancer patients, but the role of SOX4 in bladder cancer tumorigenesis is not well understood. Given SOX4’s many roles in embryonic development and context-dependent regulation of gene expression, we sought to understand SOX4’s contribution to bladder cancer and to elucidate SOX4 regulated genes that might contribute to tumorigenesis. We employed a CRISPR interference (CRISPRi) method to transcriptionally repress SOX4 expression in T24 bladder cancer cell lines, rescued these cell lines with lentivirally expressed SOX4, and performed whole genome expression profiling. SOX4 knockdown cells exhibited decreased invasive capabilities but no changes in migration or proliferation, while rescue with SOX4 lentiviral vector restored the invasive phenotype. Gene expression profiling revealed 173 high confidence SOX4 regulated genes

2018-08-16 | GSE118572 | GEO

Expression data from bladder cancer cells T24 - treated with G9a siRNA or negative control siRNA

Project description:Target genes regulated by G9a in bladder cancer cells T24 In this dataset, we include the expression data obtained from bladder cancer cells T24 treated with G9a siRNA or negative control siRNA. These data are used to obtain genes that are differentially expressed in response to G9a konckdown.

2019-05-29 | GSE115341 | GEO

RNA-Seq analysis of bladder cancer cells after protodioscin treatment

Project description:We performed RNA-seq analysis using different bladder cancer cell lines (5637 and T24) after protodioscin treatment. We reported that protodioscin regulates MAPK pathway-associated genes in 5637 and T24 cells. Protodioscin induces apoptosis and suppresses cell cycle progression, cell migration and invasion in 5637 and T24 cells.

2024-08-30 | GSE212328 | GEO

Expression data from bladder cancer cells T24 treated with ox-LDL or vehicle

Project description:Target genes regulated by ox-LDL treatment in bladder cancer cells T24 were identified by microarrays. In this dataset, we include the expression data obtained from bladder cancer cells T24 starved with serum-free medium and then treated with 20 μg/mL ox-LDL or vehicle for 24 h. These data are used to obtain genes that are differentially expressed in response to ox-LDL treatment.

2022-02-18 | GSE134530 | GEO

RNA-seq of miR-146a-5p overexpressing T24 human bladder cancer cells

Project description:We established stable miR-146a-5p overexpression T24 cells, then performed transcriptome profiling of miR-146a-5p overexpressing cells compared to control T24 cells to detect the molecular mechanisms of the miR-146a-5p’s effect on bladder cancer cells.

2024-02-03 | GSE166139 | GEO

Characterization of the difference of mRNA and lncRNA profiling between cisplatin-resistance and regular T24 bladder cancer cells

Project description:To investigate the difference of mRNA and lncRNA profiling between cisplatin-resistance and regular T24 bladder cancer cells, T24 cells were treated with a gradual increment (4, 8, 16, 32, 64 ug/ml cisplatin) with a discontinuous period until cells recover. 10^6 cells T24R and T24 cells were harvested for RNA-seq.

2019-11-11 | E-MTAB-7437 | biostudies-arrayexpress

Gene expression profileing of DDR1 overexpression and control T24 human bladder cancer cell line

Project description:We performed RNA-seq analysis on xenograft mouse model generated by T24 human bladder cancer cell line with enforced expression of DDR1 or controls.

2022-10-19 | GSE191097 | GEO

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