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CircPTK2/PABPC1/SETDB1 axis promotes EMT-mediated tumor metastasis and Gemcitabine resistance in bladder cancer

ABSTRACT: To elucidate the specific mechanism by which circPTK2 exerts oncogene functions, we screened the transcriptome by RNA-Seq, focusing on the differential expressed genes in UM-UC-3 and T24 cells with silenced circPTK2 compared to control cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE216692 | GEO | 2023/01/01

REPOSITORIES: GEO

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Altered expression of genes in WDR5 inhibited (by OICR-9429) bladder cancer cells

Project description:To explore the molecular mechanism underlying OICR-9429-induced WDR5 inhibition in BCa cells, a genome-wide RNA-sequencing was conducted to compare gene expression profiles between OICR-9429 treated T24, UM-UC-3 cells and their control cells

2021-06-24 | GSE145158 | GEO

N-acetyltransferase 10 drives cisplatin chemoresistance by enhancing ac4C-associated DNA repair in bladder cancer

Project description:To explore the molecular mechanism underlying NAT10-mediated cisplatin resistance in bladdder cancer, a genome-wide RNA-sequencing was conducted to compare gene expression profiles of T24 and UM-UC-3 cells with NAT10 knockdown and control. And acRIP-seq was performed to identified the downstream targets of NAT10.

2022-04-07 | GSE200285 | GEO

HSF1 facilitates lymphatic metastasis of bladder cancer via a novel PRMT5-WDR5-dependent transcriptional program

Project description:To further identify the underlying mechanisms of HSF1 in LN metastasis, we performed genome-wide RNA expression profile screening in which we compared gene expression profiles in HSF1-knockdown and control T24 cells To further identify the underlying mechanisms of HSF1 in LN metastasis, we performed genome-wide RNA expression profile screening in which we compared gene expression profiles in HSF1-knockdown and control UM-UC-3 cells

2021-10-22 | GSE185986 | GEO

The investigational Aurora kinase A inhibitor MLN8237 induces defects in cell viability and cell cycle progression in mouse bladder cancer cells in vitro and in vivo

Project description:PURPOSE: Despite over 70,000 new cases of bladder cancer in the United States annually, patients with advanced disease have a poor prognosis due to limited treatment modalities. We evaluate the role of Aurora A, identified as an upregulated candidate molecule in bladder cancer, in regulating bladder tumor growth. EXPERIMENTAL DESIGN: Gene expression in human bladder cancer samples was evaluated using RNA microarray and reverse-transcriptase PCR. The specific Aurora kinase A inhibitor MLN8237 (Millennium) was used to determine effects on bladder cancer cell growth using in vitro and in vivo models using malignant T24 and UM-UC-3 and papilloma-derived RT4 bladder cells. RESULTS: Urothelial carcinoma upregulates a set of 13 mitotic spindle associated transcripts, as compared to normal urothelium, including MAD2L1 (7.6-fold), BUB1B (8.8-fold), Aurora kinases A (5.6-fold) and Aurora kinase B (6.2-fold). Application of MLN8237 (10nM-1µM) to the human bladder tumor cell lines T24 and UM-UC-3 induced dose-dependent G2 cell cycle arrest, aneuploidy, mitotic spindle abnormalities, and apoptosis. MLN8237 arrested tumor growth when administered orally over 4 weeks in a mouse bladder cancer xenograft model (p<0.05). Finally, in vitro combination of MLN8237 with either paclitaxel or gemcitabine produced schedule-dependent synergistic antiproliferative effects in T24 cells when administered sequentially. CONCLUSIONS: Mitotic spindle checkpoint dysfunction is a common characteristic of human urothelial carcinoma, and can be exploited with pharmacologic Aurora A inhibition. Future studies that explore the mechanisms of spindle checkpoint failure in bladder cancer and evaluate the therapeutic role of Aurora kinases for bladder cancer patients would be of value.

2013-05-01 | GSE42089 | GEO

The investigational Aurora kinase A inhibitor MLN8237 induces defects in cell viability and cell cycle progression in mouse bladder cancer cells in vitro and in vivo

2013-05-01 | E-GEOD-42089 | biostudies-arrayexpress

Epigenome analysis of parental (native) and 3-bromopyruvate-resistant UM-UC-3 bladder cancer cells

Project description:Genome-wide DNA methylation profiling of parental (native) and 3-bromopyruvate-resistant UM-UC-3 bladder cancer cells. The Illumina Infinium 450k Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across approximately 450,000 CpGs in treatment-naive and 3-bromopyruvate-resistant UM-UC-3 bladder cancer cells.

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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

Identification of the possible molecules by which acquired platinum resistance induces EMT-like changes in urothelial carcinoma

Project description:To identify the possible targets in EMT-acquisition after developing acquired platinum resistance in urothelial carcinoma (UC), we examined the changes in global gene expression before and after development of acquired platinum resistance. Comparing two types of acquired platinum resistant UC cells and their corresponding parent cells, in the end we identified 49 genes (25 up-regulated and 24 down-regulated genes) which were commonly changed in two acquired platinum resistant UC cells. Four invasive UC cell lines, T24, 5637, and those acquired platinum-resistant sublines T24PR and 5637PR, were used for microarrays. T24PR and 5637PR cells were newly established in our laboratory, which were grown and passaged upon reaching confluence in medium containing CDDP over a 6-month period. In preliminary studies, we found that these cell lines had an altered phenotype with morphologic and molecular changes consistent with EMT, and exhibited a marked difference in migratory potential before and after developing platinum resistance.

2016-07-01 | E-GEOD-58624 | biostudies-arrayexpress

Expression profile of lncRNAs in CSCs and non-CSCs of bladder cancer cell line

Project description:Bladder cancer stem cells (CSCs) contribute to tumorigenesis, recurrence and chemoresistance of bladder cancer. However, the molecular mechanisms underlying their self-renewal are poorly unknown. Long noncoding RNAs (lncRNAs) act as crucial regulators in a lot of human cancers, yet their potential roles and molecular mechanisms in bladder CSCs are poorly understood. The goal of this study is to identify the differentially expressed lncRNAs in bladder CSCs (UM-UC-3 4th spheres), its two differentiation sublines and bladder non-CSCs (UM-UC-3). Our study reveals that deregulation of lncRNAs is involved in the bladder CSCs.

2019-09-22 | GSE107857 | GEO

NONO-mediated alternative splicing of SETMAR inhibits lymphatic metastasis in bladder cancer

Project description:To explore the molecular mechanism underlying NONO-mediated lymphatic metastasis inhibition in bladder cancer, a genome-wide RNA-sequencing was conducted to compare gene expression profiles of UM-UC-3 cells with NONO knockdown and control.

2020-03-21 | GSE147323 | GEO

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