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MiR-29 mimic and inhibitor expression in the clear cell renal cell carcinoma cell lines 786-O, A-498 and ACHN

ABSTRACT: miR-29 mimic and inhibitor expression in the clear cell renal cell carcinoma cell lines 786-O, A-498 and ACHN

PROVIDER: PRJNA606019 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11066908_1.fastq.gz	Fastqsanger.gz
	SRR11066908_2.fastq.gz	Fastqsanger.gz
	SRR11066909_1.fastq.gz	Fastqsanger.gz
	SRR11066909_2.fastq.gz	Fastqsanger.gz
	SRR18964447_1.fastq.gz	Fastqsanger.gz

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miR-29 mimic and inhibitor expression in the clear cell renal cell carcinoma cell lines 786-O, A-498 and ACHN

Project description:The goal of this study was to investigate the regulatory events underlying post-transcriptional changes in gene expression in cancer. We observed that the miR-29 regulon had reccurently increased mRNA stability across multiple cancer types and hypothesized that its down-regulation is responsible at least in part for alterations in the cancer transcriptome. To verify if restoring miR-29 activity can partially reverse these changes, we expressed a miR-29 mimic in the 786-O and A-498 clear cell renal cell carcinoma (ccRCC) lines and performed RNA-sequencing on extracted RNA. We computed differential gene expression in the cell lines expressing the miR-29 mimic, compared to the control sample. We observed that expression of miR-29 mimic partially shifts the transcriptome of cells toward a normal cell state, primarily by down-regulating the majority of genes that are up-regulated in ccRCC tumors, most of which are also miR-29 targets. We observed opposite trends when expressing a miR-29 inhibitor in the ACHN ccRCC cell line. The results suggest that miR-29 downregulation is responsible for changes in the mRNA stability of a considerable number of genes in ccRCC, which can be partially rescued when miR-29 activity is restored.

2022-07-19 | GSE145088 | GEO

Identifying lincRNA as prognostic biomarker for clear cell renal cell carcinoma

Project description:RNA sequencing libraries were made for A-498 and 786-O to detect the transcripts regulated by the lincRNA comparing knockdown and the non-targeting control.

2016-12-31 | GSE70602 | GEO

786-O and 786-VHL in EMCV study

Project description:786-0 is a cell line derived from a clear cell renal carcinoma. Previous studies have shown that the 786-O cell line harbors an inactivating mutation in the von-Hippel Lindau (VHL) gene. Mutations in the VHL gene occur in the majority of sporadic clear cell renal cell. To determine how inactivation of the VHL affects cellular functions, we created a derivative of 786-0, which we call 786-VHL in which a functional allele of VHL has been introduced back into the 786-O cell line. The renal cell carcinoma cell line 786-0, which harbors a mutated allele of VHL, was compared to a cell line derived from 786-0, termed 786-VHL, that contains a functional allele of VHL. Genes whose expression characteristics were dependent on functional VHL were identified.

2010-06-23 | E-GEOD-22256 | biostudies-arrayexpress

786-O and 786-VHL in EMCV study

2010-06-10 | GSE22256 | GEO

Genome-wide mapping of HIF-2 binding in 786-O clear cell renal carcinoma cells

Project description:Kidney cancer accounts for more than 100,000 deaths per year world-wide. More than 80% are clear cell tumors (ccRCCs) and the majority are associated with loss of function of the von Hippel Lindau (pVHL) tumor suppressor resulting in upregulation of HIF-{alpha} subunits, and activation of HIF-dependent transcriptional pathways. Recent GWAS studies have discovered RCC-susceptibility loci both within EPAS1 (HIF-2{alpha}) and in an intergenic region of unknown function on 11q13.3. As part of an ongoing study to define the direct transcriptional targets of HIF-2 in renal cancer, we undertook a genome-wide analysis of HIF-2-binding sites in pVHL-defective 786-O cells (that lack functional HIF-1{alpha} due to a truncated transcript) using chromatin immunoprecipitation with antibodies directed against HIF-2{alpha} and its dimerization partner HIF-1{beta}, coupled to high-throughput sequencing (ChIP-seq). Amongst approximately 600 pangenomic HIF-2{beta} ChIP signals, we observed strong binding (ranked 12th by peak height) almost precisely coinciding with the RCC predisposition SNP rs7105934 on 11q13.3. We report binding of HIF-2{alpha} and HIF-1{beta} in 786-O clear cell renal carcinoma cells. 3 samples examined, HIF-2{alpha}, HIF-1{beta} and pre-immune control ChIP.

2012-02-01 | E-GEOD-34871 | biostudies-arrayexpress

Sinorhizobium meliloti strain:498

Project description:Sinorhizobium meliloti 498 Resequencing

| PRJNA501542 | ENA

786-0 renal cell carcinoma cell line Everolimus treatment

Project description:We present transcriptome profiling of 786-0 renal cell carcinoma cell lines both with and without Everolimus, an mTOR inhibitorhbn

2022-12-01 | GSE99875 | GEO

Rhizobium leguminosarum strain:SEMIA 498 | isolate:SEMIA 498

Project description:Rhizobium leguminosarum SEMIA 498 genome sequencing

| PRJNA581087 | ENA

Treatment of renal cell carcinoma cell line A-498 with zebularine

Project description:Cultures of A-498 cells were treated for 120hours with 1000ÂµM zebularine (SIGMA) in three independent biological experiments. Zebularine acts as a DNA methyltransferase (DNMT) inhibitor thereby upregulating genes that are inactivated by e.g. promotor hypermethylation. The experiment aimed to search for upregulated transcripts to provide new targets for biomarker development and therapeutic use. 308 candidates were upregulated more than 1.5-fold. Members of the metallothionein group (MT1G, MT1H, and MT2A) were validated in 49 clinical samples of renal cell carcinomas. Total RNA of treated (1000ÂµM zebularine) and untreated A-498 cells (experiment A05-A07) was subjected to Affymetrix array analysis to detail the overall expression changes after treatment with a DNMT inhibitor. Treated cells showed no obvious signs of zebularine-induced cytotoxicity as revealed by XTT assays. Cell were split twice during the 120hour treatment period.

2013-10-24 | E-GEOD-51627 | biostudies-arrayexpress

Cooperative blockade of CK2 and ATM kinases drives apoptosis in VHL-deficient renal carcinoma cells / RNA-seq (BRB-seq) of treated 786-O spheroids

Project description:Multicellular Tumor Spheroids (MCTS) were pre-formed for 3 days with 786-O cell line to better mimic the tumor microenviroenment. These spheroids were treated with either vehicle (DMSO), drugs alone (KU-60019 10 μM; CX-4945 5 μM) or in combination (KU + CX) for 48h before RNA extraction.

2021-02-04 | E-MTAB-9977 | biostudies-arrayexpress

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