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ABSTRACT: RNA sequencing data of bladder cancer 5637 cell line

PROVIDER: PRJNA1184403 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31304100_1.fastq.gz	Fastqsanger.gz
	SRR31304100_2.fastq.gz	Fastqsanger.gz
	SRR31304101_1.fastq.gz	Fastqsanger.gz
	SRR31304101_2.fastq.gz	Fastqsanger.gz
	SRR31304102_1.fastq.gz	Fastqsanger.gz

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Transcriptomic analysis of 5637 bladder cancer cell line transfected with MAT1A plamid, 48 hours post transfection

Project description:Transcriptomic analysis of 5637 bladder cancer cell line transfected with MAT1A plamid, 48 hours post transfection

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Chromatin Profiling of 5637 bladder cancer cell line

Project description:Chromatin Profiling of 5637 bladder cancer cell line

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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.

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Proteomic analysis of the invasiveness of human bladder cancer cells

Project description:To identification of key drivers involved in the development of muscle invasive bladder cancer, which displays poor prognosis, we isolated one subpopulation of human 5637 bladder cancer cells with highly invasiveness and the other subpopulation of 5637 cells with low invasiveness by Transwell method. Through proteomic analysis, differentially expressed proteins were displayed.

2018-03-15 | PXD007709 | Pride

Chromatin Profiling of 5637 bladder cancer cell line

Project description:In order to investigate epigenetic landscape and potential alterations in bladder, we established the chromatin profiling of 5637 cell line by ChIPseq for the following marks and transcription factor : H3K4me3, H3K9ac, H3K27me3, H3K9me3, H3K27ac, H3K4me1, CTCF and FOXA1.

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Identification of a novel set of DNA methylation markers in bladder cancer using MBD-methylCap/seq and urine DNA screening in a Chinese population

Project description:The aim of the present study was to identify novel DNA methylation markers in bladder cancer (BCa) through genome-wide profiling of bladder cancer cell lines and subsequent MSP screening in urine samples. Experimental Design: MBD methylCap/seq was carried out to screen differentially methylated CpG islands using two BCa cell lines (5637 and T24) and two normal bladder mucosa (BM) samples. The top one hundred most hypermethylated targets were screened using Methylation Specific PCR (MSP) in small and big cohort of urine samples from BCa patients and normal controls. The diagnostic performance of the gene panel was further evaluated in different clinical scenarios. Results: In total, 1,627 gene promoter regions hypermethylated in BCa cell line were identified in genomic level methylation profiling. The followed screening procedure in clinical urine sample generated eight genes (VAX1, KCNV1, ECEL1, TMEM26, TAL1, PROX1, SLC6A20, and LMX1A) capable of differentiating BCa from normal control. Subsequent validation in a large sample size enabled the optimisation of 5 methylation targets (VAX1, KCNV1, TAL1, PPOX1 and CFTR) for BCa diagnosis with sensitivity and specificity of 86.32% and 87.13%, respectively. In addition, VAX1 and LMX1A methylation could predict the tumour recurrence. Conclusions: Tumor specific biomarkers of BCa could be established by first performing genome level methylation profiling with cell lines and then screening the potential targets in urine samples. The panel of methylated genes identified was promising for the early non-invasive detection and surveillance of BCa. MBD methylCap/seq was carried out to screen differentially methylated CpG islands using two BCa cell lines (5637 and T24), and two normal bladder tissue mix as control.

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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.

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