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HSF1 activates ANXA11-mediated glutamine metabolism by super enhancer long non-coding RNA LINC00857 in colorectal cancer [array]

ABSTRACT: HSF1 activates ANXA11-mediated glutamine metabolism by super enhancer long non-coding RNA LINC00857 in colorectal cancer [array]

PROVIDER: PRJNA814243 | ENA |

REPOSITORIES: ENA

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HSF1 activates ANXA11-mediated glutamine metabolism by super enhancer long non-coding RNA LINC00857 in colorectal cancer [array]

Project description:We shed light on a closely cooperative machinery between HSF1 and super enhancer for the first time in CRC. HSF1 could stimulate super enhancer activity by the enrichment of acetyltransferase P300 to LINC00857 promoter region, contributing to LINC00857 transcription.

2022-08-15 | GSE198224 | GEO

HSF1 activates ANXA11-mediated glutamine metabolism by super enhancer long non-coding RNA LINC00857 in colorectal cancer [ChIP-seq]

2022-08-15 | GSE198223 | GEO

HSF1 activates ANXA11-mediated glutamine metabolism by super enhancer long non-coding RNA LINC00857 in colorectal cancer.

Project description:HSF1 activates ANXA11-mediated glutamine metabolism by super enhancer long non-coding RNA LINC00857 in colorectal cancer.

| PRJNA814242 | ENA

HSF1 activates ANXA11-mediated glutamine metabolism by super enhancer long non-coding RNA LINC00857 in colorectal cancer [ChIP-seq]

Project description:HSF1 activates ANXA11-mediated glutamine metabolism by super enhancer long non-coding RNA LINC00857 in colorectal cancer [ChIP-seq]

| PRJNA814244 | ENA

HSF1 activates ANXA11-mediated glutamine metabolism by super enhancer long non-coding RNA LINC00857 in colorectal cancer.

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-08-15 | GSE198225 | GEO

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

Expression data from Saccharomyces cerevisiae WT, WT(hsf1), hac1delta and hac1delta(hsf1)

Project description:In the yeast Saccharomyces cerevisiae, accumulation of misfolded proteins in the endoplasmic reticulum (ER) causes ER stress and activates the unfolded protein response (UPR) mediated by Hac1p, whereas the heat shock response (HSR) mediated by Hsf1p mainly regulates cytosolic processes and protects the cell from different stresses. In this study, we find that a constitutive activation of the HSR by over-expression of a mutant HSF1 gene could relieve ER stress in both wild type and hac1delta UPR-deficient cells. We studied the genome-wide transcriptional response in order to identify regulatory mechanisms that govern the interplay between UPR and HSR responses. Interestingly, we find that the regulation of ER stress via HSR is mainly through facilitation of protein folding and secretion and not via the induction of Rpn4-dependent proteasomal activity. Four Saccharomyces cerevisiae strains, WT, WT(hsf1), hac1delta and hac1delta(hsf1), were grown in SD-URA medium and treated with 2.5 mM DTT. After two hours induction, samples were taken for RNA extraction and hybridization on Affymetrix microarrays. Biological triplicates were applied.

2014-07-01 | E-GEOD-39311 | biostudies-arrayexpress

HSF1 Stimulates Glutamine Transport by Super-Enhancer-Driven lncRNA LINC00857 in Colorectal Cancer.

Project description:Super enhancers are critical for the gene transcription responsible for cell fate by interacting with transcription factors. However, the relevance of HSF1 to super enhancers in tumors remains obscure. We profiled H3K27ac enrichment by chromatin immunoprecipitation sequencing. HSF1-mediated lncRNAs were identified by lncRNA microarray. The characteristics of LINC00857 were explored by in vitro and in vivo assays. The mechanism was studied via chromatin immunoprecipitation, RNA immunoprecipitation, and HSF1/ANXA11 knockout mice. We found that super enhancers occupied multiple gene loci in colorectal cancer. We screened out an HSF1-mediated super enhancer, lncRNA-LINC00857, which exerts its characteristics in promoting cell growth via regulating glutamine metabolism. Notably, HSF1 could stimulate the super-enhancer activity of LINC00857 by the enrichment of acetyltransferase P300 to its gene loci, contributing to LINC00857 transcription. In turn, nuclear LINC00857 cooperated with HSF1 to promote ANXA11 transcription, which modulated SLC1A5/ASCT2 protein expression by binding competitively to miR-122-5p. The knockout of ANXA11 attenuated colorectal cancer formation in vivo. Collectively, we shed light on a closely cooperative machinery between HSF1 and super enhancers. HSF1 could stimulate acetyltransferase P300-mediated super-enhancer activity to facilitate LINC00857 expression, contributing to SLC1A5-mediated glutamine transport. Targeting the HSF1/LINC00857/ANXA11 axis may provide a valuable therapeutic strategy against colorectal cancer.

| S-EPMC9406190 | biostudies-literature

Genome-wide characterization of HSF1 binding in human WT and FBXW7 KO colon cancer cells under basal conditions and upon heat shock

Project description:FBXW7 modulates stress response by post-translational modification of HSF1 HSF1 orchestrates the heat-shock response upon exposure to heat stress and activates a transcriptional program vital for cancer cells. In this study we assayed for genome-wide localization of HSF1 enrichment in the HCT116 FBXW7 KO colon cells and their wild type counterpart in untreated cells and upon heat shock. These results revealed that accumulation of nuclear HSF1 in FBXW7 KO cells results in rewiring of the HSF1 transcriptional program. Five 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-57398 | biostudies-arrayexpress

Genome-wide characterization of HSF1 binding in human WT and FBXW7 KO colon cancer cells under basal conditions and upon heat shock

2015-02-20 | GSE57398 | GEO