Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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

ORGANISM(S): Homo sapiens

PROVIDER: GSE185986 | GEO | 2021/10/22

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

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

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

| PRJNA771657 | ENA

Yeast HSF1 vs hsf1-ba1

Project description:Upon heat shock, Hsf1 protein is extensively phosphorylated, however, this modification is inhibited by an hsf1-bal mutation. To get genome-wide effect of the hyperphosphorylation on Hsf1-regulated transcription, the heat-induced gene expression profiles in HSF1 and hsf1-bal cells were compared. Keywords: stress response

2005-09-27 | GSE3361 | GEO

Gene expression profiling in HSF1-knockdown human oral squamous cell carcinoma HSC-3 cells

Project description:Heat shock transcription factor 1 (HSF1) is recognized as the major regulator of the heat shock transcriptional response, and also plays a central role in the cellular functions of cancer cells. Here, to identify the molecular mechanism by which HSF1 regulates the proliferation of cancer cells, comparative gene expression analysis was performed with mock and HSF1-knockdown cells. Silencing of HSF1 in human oral squamous cell carcinoma HSC-3 cells was carried out by siRNA technology and the expression of HSF1 was confirmed by Western blotting. Gene expression was analyzed using GeneChip oligonucleotide microarrays and computational gene expression analysis tools. HSF1 knockdown significantly decreased the number of viable cells. Of the 54,675 probe sets analyzed, 221 probe sets were up-regulated and 423 probe sets were down-regulated by >2-fold in HSF1-knockdown cells.

2012-05-23 | GSE38058 | GEO

Gene expression profiling in HSF1-knockdown human oral squamous cell carcinoma HSC-3 cells

2012-05-22 | E-GEOD-38058 | biostudies-arrayexpress

Genome-wide characterization of HSF1 binding in human 451Lu melanoma cancer cells under basal conditions

Project description:HSF1 orchestrates a transcriptional program vital for cancer cells. In this study we assayed for genome-wide localization of HSF1 enrichment in the 451Lu melanoma in untreated cells. These results revealed a transcriptional program enriched for metastasis-related genes. Twenty million cells were used for the ChIP and precipitated using 5 micrograms of antibody (cell signaling, 4356) against human HSF1

2015-02-20 | E-GEOD-63589 | biostudies-arrayexpress

Identification of targets regulated by HSF1 in response to HSP90 inhibitors

Project description:A375 cells with inducible knockdown HSF1 with and without HSP90 inhibitor treatment

2013-03-06 | GSE44867 | GEO

Genome-wide characterization of HSF1 binding in human 451Lu melanoma cancer cells under basal conditions

2015-02-20 | GSE63589 | GEO

Tumor metastasis to lymph node requires YAP-dependent metabolic adaptation

Project description:In cancer patients, metastasis of tumors to sentinel lymph nodes (LN) predicts disease progression and often guides treatment decisions. The mechanisms underlying tumor LN metastasis are poorly understood. Using comparative transcriptomics and metabolomics analyses of primary and LN metastatic tumors in mice, we found that LN metastasis requires that tumor cells undergo a metabolic shift toward fatty acid oxidation (FAO). Transcriptional co-activator yes-associated protein (YAP) is selectively activated in LN metastatic tumors, leading to upregulation of genes in the FAO signaling pathway. Pharmacological inhibition of FAO or genetic ablation of YAP suppressed LN metastasis in mice. Several bioactive bile acids were highly accumulated in the LN metastatic tumor. Inhibition of FAO or YAP may merit exploration as therapeutic strategies for mitigating tumor LN metastasis.

2019-02-09 | E-MTAB-7621 | biostudies-arrayexpress

Transcription profiling of human heat shocked HeLa cell line with siRNA knockdown of HSF1

Project description:Although HSF1 is known to play an important role in regulating the cellular response to proteotoxic stressors, little is known about the structure and function of the HSF1 signaling network under both stressed and unstressed conditions. In this study, we used a combination of chromatin immunoprecipitation (ChIP) microarray analysis and time course gene expression microarray analysis with and without siRNA-mediated inhibition of HSF1 comprehensively identify genes directly and indirectly regulated by HSF1 and examine the structure of the extended HSF1 signaling network. Correlation between promoter binding and gene expression was not significant for all genes bound by HSF1 suggesting that HSF1 binding per se is not sufficient for expression. However, the correlation with promoter binding was significant for genes identified as HSF1-regulated following siRNA knockdown allowing the identification of direct transcriptional targets of HSF1. Among promoters bound by HSF1 following heat shock, a gene ontology (GO) analysis showed significant enrichment only in categories related to protein folding. In contrast, analysis of the extended HSF1 signaling network showed enrichment in a variety of categories related to protein folding, anti-apoptosis, RNA splicing, ubiquitination and others, highlighting a complex transcriptional program directly and indirectly regulated by HSF1.,SUBMITTER_CITATION: Genome-wide analysis of human HSF1 signaling reveals a transcriptional program linked to cellular adaptation and survival Authors: Todd J. Page, Devanjan Sikder, Longlong Yang, Linda Pluta, Russell D. Wolfinger, Thomas Kodadek, and Russell S. Thomas Journal: Molecular Biosystems 2:627-639

2007-06-22 | E-GEOD-3697 | biostudies-arrayexpress

Characterizing an HSF1-dependent transcriptional program in metastatic lung adenocarcinoma

Project description:The purpose of this study was to identify gene targets differentially regulated by shRNA-mediated knockdown of the HSF1 transcription factor in the brain-metastatic lung adenocarcinoma cell line PC9-BrM3.

2021-01-06 | GSE149246 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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