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Genome-wide DNA methylation maps of Decitabine and/or Cisplatin treated bladder cancer cells.

ABSTRACT: Genome-wide DNA methylation maps of Decitabine and/or Cisplatin treated bladder cancer cells.

PROVIDER: PRJNA451473 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7057530.fastq.gz	Fastqsanger.gz
	SRR7057531.fastq.gz	Fastqsanger.gz
	SRR7057532.fastq.gz	Fastqsanger.gz
	SRR7057533.fastq.gz	Fastqsanger.gz
	SRR7057534.fastq.gz	Fastqsanger.gz

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Similar Datasets

Genome-wide DNA methylation maps of Decitabine and/or Cisplatin treated bladder cancer cells.

Project description:It is well established that low-dose Decitabine treatment can sustain long-term antitumor effects by targeting DNA methylation and altering gene expression32. We performed methylated DNA immunoprecipitation (MEDIP) followed by next-generation sequencing in 5637 cells. Daily Decitabine treatment with 100 nM for 72 hr (with or without 100ng/ml cisplatin treatment) reduced the methylation level at CpG-islands in the genome of 5637 cells . However, this low-dose DEC treatment did not cause a significant reduction of DNA methylation in non-CpG islands regions.Our study represents the first detailed analysis of DNA methylome generated by RNA-seq technology in bladder cancer cells treated with low-dose decitabine. This study help to reveal the direct target genes of decitabine in bladder cancer treatement.

2021-04-23 | GSE113537 | GEO

The STAT3 induced ITGB4 overexpression represses p53 to reduce the sensitivity of bladder cancer to cisplatin

Project description:Cisplatin-based chemotherapy is the first-line treatment for patients with advanced bladder cancer, but the development of cisplatin-resistance limits its anti-tumor effects. Previous studies have shown that cisplatin resistance in bladder cancer may be related to a variety of factors, such as changes in drug transport and metabolism, enhancement of DNA repair mechanisms, changes in cell cycle regulation, inhibition of apoptosis, and epigenetic modification. While, the mechanism of cisplatin resistance is still elusive.In this study, we first found that upregulated ITGB4 is correlated with poor prognosis after chemotherapy in bladder cancer. Next, we demonstrated ITGB4 plays a key role in regulating the sensitivity of bladder cancer to cisplatin therapy. Then, we found that ITGB4 reduced the sensitivity of bladder cancer to cisplatin by inhibiting p53-S15 site phosphorylation and promoting MDM2 binding to p53 to reduce p53 expression. In addition, we demonstrated that ITGB4 regulates the antitumor effects of MDM2 inhibitors combined with cisplatin therapy. Further, we found that ITGB4 was elevated in bladder cancer cisplatin-resistant cells, and the increase in ITGB4 was mediated by STAT3.The combination of STAT3 inhibitors can enhance the antitumor effect of cisplatin in bladder cancer.In summary, we identified ITGB4 as a key molecule affecting cisplatin sensitivity in bladder cancer, and proposed a strategy of combining drugs with STAT3 inhibitors to increase cisplatin sensitivity in bladder cancer.

2024-06-07 | GSE268855 | GEO

APIM-peptide targeting PCNA improves cisplatin therapy in a rat muscle-invasive bladder cancer model

Project description:High mortality rate of muscle-invasive bladder cancer (MIBC) and complexity of disease demand new multi-targeting treatment strategies. Targeting proliferating cell nuclear antigen (PCNA) with a peptide containing the AlkB homologue 2 PCNA interacting motif (APIM), is shown to impair multiple vital cellular stress responses and induce hypersensitivity against several chemotherapeutics in different pre-clinical models. This study examine the anti-cancer efficacy of the novel APIM-peptide drug when combined with cisplatin-based therapies (cisplatin, cisplatin/gemcitabine (GC) and methotrexate/vinblastine/adriamycin/cisplatin (MVAC)) in a panel of bladder cancer (BC) cells and with intravenous cisplatin-therapy in a rat MIBC-model. Furthermore, we explore the molecular mechanisms underlying the observed effects on a genomic, proteomic and metabolomic level using microarray, multiplexed inhibitor bead (MIB)-assay, and targeted mass spectrometric metabolite profiling. The APIM-peptide significantly increased the efficacy of all cisplatin-based therapies in all BC cell lines tested, including a cisplatin resistant cell line and reduced the tumor load in cisplatin treated MIBC-bearing rats. Genome and proteome analysis of APIM-peptide/cisplatin treated BC cells revealed reduced expression of multiple proteins frequently overexpressed in MIBC. Of notice, the EGFR/ERBB2, PI3K/Akt and MAPK signaling pathways and anti-apoptosis were downregulated. We suggest that the anti-cancer effect of the APIM-peptide is through the downregulation of several known oncogenic signaling pathways including anti-apoptosis. Together our results indicate that the APIM-peptide represents a potential improved treatment approach for patients with MIBC.

2018-09-10 | PXD008724 | Pride

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

Genome-wide methylation and expression profiling study identifies candidate DNA methylation drivers of acquired cisplatin resistance in ovarian cancer.

Project description:This SuperSeries is composed of the following subset Series: GSE28646: Gene expression profiling in A2780, CP70 and CP70 following Decitabine and/or PXD101 treatment GSE28647: Genome-wide methylation profiling identifies candidate DNA methylation drivers of acquired cisplatin resistance in ovarian cancer. Refer to individual Series

2011-12-20 | E-GEOD-28648 | biostudies-arrayexpress

Activation of cGAS-STING signal to inhibit the proliferation of bladder cancer: the immune effect of cisplatin

Project description:our findings indicated a cisplatin dependent cGAS-STING signal in bladder cancer. This signal could be enhanced by accumulation of dsDNA and chromatin dissociated cGAS and would finally recruit infiltration DCs and CD8+ T cells in bladder cancer bladder cancer tumor microenvironment. However, the specific role and effect of this signal towards bladder cancer tumor microenvironment need to be further clarified.

2021-03-31 | GSE165767 | GEO

Reprogrammed Lipid Metabolism in Bladder Cancer with Cisplatin Resistance

Project description:This study conducted comprehensive and comparative lipidomic profiling of two isogenic human T24 bladder cell lines, which are characterized as sensitive or resistant to the cisplatin-induced cell apoptosis.

2017-04-10 | ST001120 | MetabolomicsWorkbench

N6-methyladenosine RNA modification drives a rapid shift to cisplatin resistance in bladder cancer by regulating SLC7A11 expression via YTHDF3 [RNA-seq]

Project description:Our study examines the role of m6A RNA modification in regulating gene expression of transcripts promoting cisplatin resistance in bladder cancer.

2023-11-08 | GSE231835 | GEO

N6-methyladenosine RNA modification drives a rapid shift to cisplatin resistance in bladder cancer by regulating SLC7A11 expression via YTHDF3 [RIP-seq]

Project description:Our study examines the role of m6A RNA modification in regulating gene expression of transcripts promoting cisplatin resistance in bladder cancer.

2023-11-08 | GSE231834 | GEO

The M1 aminopeptidase NPEPPS is a novel regulator of cisplatin sensitivity

Project description:Platinum-based chemotherapeutics are used in many combination regimens in cancer. Despite extensive use across diverse cancer types, there is room for improved efficacy and patient selection for treatment. Here, we use bladder cancer to address both issues. A multi-omic assessment of five human bladder cancer cell lines and their chemotherapy resistant derivatives, coupled with in vitro whole-genome CRISPR screens were used to define functional drivers of treatment resistance. We identified 46 genes that sensitized the resistant cell lines to cisplatin plus gemcitabine (GemCis), a standard combination therapy in bladder cancer. Most genes were involved with DNA damage and repair pathways, which have previously been associated with enhanced sensitivity to cisplatin. Evaluating expression of the 46 genes in the whole transcriptome and proteome data in parental and resistant lines identified the puromycin sensitive aminopeptidase, NPEPPS, as a novel hit. Depletion of NPEPPS resulted in sensitizing resistant bladder cancer cells to cisplatin in vitro and in xenograft experiments. Pharmacologic inhibition of NPEPPS with tosedostat in cells and in chemoresistant, bladder cancer patient-derived tumoroids improved response to cisplatin. Prior work found NPEPPS in a protein complex with volume regulated anion channels (VRACs) in several cell line models. Interestingly, depletion of two VRAC subunits, LRRC8A and LRRC8D, known importers of intracellular cisplatin, enhanced resistance to cisplatin. Our findings support NPEPPS as a novel and druggable driver of cisplatin resistance with the potential for rapid translation to clinical investigation.

2024-02-20 | PXD024742 | Pride

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