Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

40 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The mechanism of elevated S100A6 (Calcyclin) Enhances Tumorigenesis in clear cell renal cell carcinoma

ABSTRACT: Among all types of urological cancers, the clear cell renal cell carcinoma is the second leading cause of death in adults. This is mainly due to lack of promising prognosis or predictors, and effective target therapy. S100A6 (calcyclin), a member of S100 family of proteins, is reported to be elevated in many types of cancers. In the present study, we analyzed the expression of S100A6 in mRNA, in proteins and tissues. The mechanism of enhancing tumorigenesis was studied to understand the role of S100A6 in clear cell renal cell carcinoma tumorigenesis. Microarray and bioinformatic analyses were performed in the stable transfection of overexpression and knockdown of S100A6, comparing with each empty vector control in order to find the different expression genes and explore the mechanism. The microarray analysis of clear cell renal cell carcinoma 786-O cell line treated with overexpression and knockdown S100A6. Four samples: overexpression S100A6 sample and vector control sample, knockdown S100A6 and vector control sample, each sample had three replicates.

ORGANISM(S): Homo sapiens

SUBMITTER: xu zhang

PROVIDER: E-GEOD-52708 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

The mechanism of elevated S100A6 (Calcyclin) Enhances Tumorigenesis in clear cell renal cell carcinoma

Project description:Among all types of urological cancers, the clear cell renal cell carcinoma is the second leading cause of death in adults. This is mainly due to lack of promising prognosis or predictors, and effective target therapy. S100A6 (calcyclin), a member of S100 family of proteins, is reported to be elevated in many types of cancers. In the present study, we analyzed the expression of S100A6 in mRNA, in proteins and tissues. The mechanism of enhancing tumorigenesis was studied to understand the role of S100A6 in clear cell renal cell carcinoma tumorigenesis. Microarray and bioinformatic analyses were performed in the stable transfection of overexpression and knockdown of S100A6, comparing with each empty vector control in order to find the different expression genes and explore the mechanism. The microarray analysis of clear cell renal cell carcinoma 786-O cell line treated with overexpression and knockdown S100A6.

2013-11-25 | GSE52708 | GEO

Normal and Renal Cell Carcinoma Kidney Tissue, Human

Project description:Each total RNA sample is hybridized to two different arrays: Affymetrix U133A (GPL96) and U133B (GPL97). For most of the normal tissue samples there is a renal clear cell carcinoma sample from the same patient. There is no matching tumor sample for normal sample N1. For most of the renal clear cell carcinoma samples there is a corresponding adjacent normal tissue sample from the same patient. There are no matching normal tissue samples for C011 or C032. Keywords = kidney Keywords = renal Keywords = RCC Keywords = carcinoma Keywords = cancer Keywords: parallel sample

2003-11-25 | GSE781 | GEO

Expression data from 786-O renal cell cancer cells treated with pentamidine

Project description:While early stages of clear cell renal cell carcinoma (ccRCC) are curable, survival outcome for metastatic ccRCC remains poor. The purpose of the current study was to apply a new individualized bioinformatics analysis (IBA) strategy to these transcriptome data in conjunction with Gene Set Enrichment Analysis of the Connectivity Map (C-MAP) database to identify and reposition FDA-approved drugs for anti-cancer therapy. We demonstrated that one of the drugs predicted to revert the RCC gene signature towards normal kidney, pentamidine, is effective against RCC cells in culture and in a RCC xenograft model. Most importantly, pentamidine slows tumor growth in the 786-O human ccRCC xenograft mouse model. To determine which genes are regulated by pentamidine in a human RCC cell line, 786-O, we treated these cells with pentamidine and performed transcriptional profiling analysis. We used microarrays to determine the set of genes regulated by pentamidine in 786-O renal cell cancer cells. Total RNA was isolated from 786-O cells treated with 25 Î¼M pentamidine or vehicle control (DMSO) for 6 hours and hybridized to Affymetrix microarrays.

2014-08-05 | E-GEOD-54709 | biostudies-arrayexpress

Transcription profiling by array of human renal carcinoma cells after EMCV or VSV infection

Project description:Comparison of gene expression in renal cell carcinoma cells after viral treatment

2010-06-18 | E-MTAB-294 | biostudies-arrayexpress

Normal and Renal Cell Carcinoma Kidney Tissue, Human

2003-11-25 | E-GEOD-781 | biostudies-arrayexpress

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

The deubiquitylating enzyme USP35 restricts regulated cell death to promote survival of renal clear cell carcinoma

Project description:The ubiquitin proteasome system governs a wide spectrum of cellular events and offers therapeutic opportunities for pharmacological intervention in cancer treatment. Renal clear cell carcinoma represents the predominant histological subtype and accounts for the majority of cancer death related to kidney malignancies. Through a systematic survey in the association of human ubiquitin-specific proteases with patient prognosis of renal clear cell carcinoma and subsequent phenotypic validation, we uncovered the tumor-promoting role of USP35. Biochemical characterizations confirmed the stabilizing effects of USP35 towards multiple members of the IAP family in an enzymatic activity-dependent manner. USP35 silencing led to reduced expression levels of IAP proteins, which were accompanied with increased cellular apoptosis. Further transcriptomic analysis revealed that USP35 knockdown altered expression levels of NRF2 downstream transcripts, which were conferred by compromised NRF2 abundance. USP35 functions to maintain NRF2 levels by catalyzing its deubiquitylation and thus antagonizing degradation. NRF2 reduction imposed by USP35 silencing rendered renal clear cell carcinoma cells increased sensitivity to ferroptosis induction. Finally, induced USP35 knockdown markedly attenuated xenograft formation of renal clear cell carcinoma in nude mice. Hence, our findings identify a number of USP35 substrates and reveal the protecting role of USP35 against both apoptosis and ferroptosis in renal clear cell carcinoma.

2023-06-17 | GSE216154 | GEO

HAVCR/KIM-1 activates the IL-6/STAT-3 Pathway in ccRCC and Determines Tumor Progression and Patient Outcome

Project description:Renal cell carcinoma (RCC), the third most prevalent urological cancer, claims more than 100,000 lives/year worldwide. The clear cell (ccRCC) is the most common and aggressive subtype of renal cancer. Commonly asymptomatic, more than 30% of ccRCCs are diagnosed when they are already metastatic resulting in a 95% mortality rate and one-third of organ-confined cancers treated by nephrectomy develop metastasis during the follow-up. Diagnosis and monitoring requires expensive and frequent imaging examinations; thereby, finding of diagnostic and prognostic biomarkers to screen, diagnose and monitor renal cancers are clearly needed. Hepatitis A virus receptor/kidney injury molecule 1 (HAVCR1/KIM-1) gene has been claimed to be a susceptibility gene for ccRCC and HAVCR1/KIM-1 ectodomain shedding a predictive biomarker of tumor progression.

2020-09-27 | E-MTAB-2071 | biostudies-arrayexpress

Project description:RNA-seq of clear renal cell carcinoma after PBRM1 knockdown

| PRJNA777891 | ENA

Somatic Mutation Screen of Clear Cell RCC II

Project description:Systematic somatic mutation screening of 4000 genes in human clear cell renal cell carcinoma. Information on corresponding somatic mutations in each sample can be found at http://www.sanger.ac.uk/genetics/CGP/Studies/.

2010-01-05 | GSE17818 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data