Expression data from Hela cells and HSF2-deficient HeLa cells subjected to heat treatment in the presence of IHSF115, an inhibitor of HSF1.
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PROVIDER: PRJNA889920 | ENA |
REPOSITORIES: ENA
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Project description:The majority of heat-induced genes were inhibited by IHSF115, i.e. were positively regulated by HSF1, suggesting that HSF1 plays a predominant role in the transcription of heat-induced genes IHSF115 effectively countermanded repression in a significant fraction of heat-repressed genes, suggesting that repression of these genes is mediated by transcriptionally active HSF1.
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Project description:Heat shock transcription factors HSF1 and HSF2 both are necessary for proper spermatogenesis, which is disrupted at elevated temperatures. We studied how HSF1 and HSF2 cooperate during the heat shock response in mouse spermatocytes. For this purpose we used ChIP-sequencing. ChIP-Seq analyses revealed that the temperature elevation induces remodeling of HSF1 and HSF2 binding to chromatin. The highest HSF1-chromatin binding was observed at 43°C, when HSF2-chromatin binding was reduced. Many promoters (mainly Hsp genes) were occupied by both heat shock factors at physiological temperature of testes and/or at 38°C. In contrary at 43°C only HSF1 was bound. Obtained results suggest that HSF1 and HSF2 could cooperate in regulation of the transcription of some genes only at physiological temperatures and/or at 38°C. Alteration in HSFs interactions and their binding to chromatin could be one of the reason of increased spermatogenic cell death observed after heat shock.
2014-10-07 | GSE56735 | GEO
Project description:Heat shock transcription factors HSF1 and HSF2 both are necessary for proper spermatogenesis, which is disrupted at elevated temperatures. We studied how HSF1 and HSF2 cooperate during the heat shock response in mouse spermatocytes. For this purpose we used ChIP-sequencing. ChIP-Seq analyses revealed that the temperature elevation induces remodeling of HSF1 and HSF2 binding to chromatin. The highest HSF1-chromatin binding was observed at 43M-BM-0C, when HSF2-chromatin binding was reduced. Many promoters (mainly Hsp genes) were occupied by both heat shock factors at physiological temperature of testes and/or at 38M-BM-0C. In contrary at 43M-BM-0C only HSF1 was bound. Obtained results suggest that HSF1 and HSF2 could cooperate in regulation of the transcription of some genes only at physiological temperatures and/or at 38M-BM-0C. Alteration in HSFs interactions and their binding to chromatin could be one of the reason of increased spermatogenic cell death observed after heat shock. On Illumina platform we sequenced DNA immunoprecipitated from isolated spermatocytes using anti-HSF1 antibody or anti-HSF2 antibody. Cells were either untreated (control) or heat shocked for 5-20 minutes. Two PCR-verified ChIP replicates were collected per each sample, and three negative control samples with normal goat serum were included.
2014-10-07 | E-GEOD-56735 | biostudies-arrayexpress
Project description:Prostate cancer (PrCa) is one of the most common malignancies in Western countries. However, the pathways that promote invasion, especially in late-stage castration-resistant PrCa (CRPC), are poorly understood. Heat shock factors (HSFs) are transcriptional regulators essential for cell survival upon proteotoxic stress, and HSF1 is also identified as a driver of oncogenesis. Here, our aim was to elucidate the molecular mechanisms that contribute to CRPC and invasion. In silico analyses showed that high HSF1 expression levels correlate with poor survival and high Gleason score in PrCa. In the same data set, HSF2, which has not previously been linked to cancer, displayed decreased expression. Using 3-dimensional (3D) organotypic PrCa cultures that spontaneously undergo an invasive conversion, opposite effects of HSF1 and HSF2 were observed; tumor spheroids lacking HSF1 grew slowly, were polarized and devoid of invasive structures, and depletion of HSF2 potentiated invasiveness. In the in vivo xenograft chorioallantoic membrane model, HSF1 silencing caused tumor regression and fibrosis, and knockdown of HSF2 generated large invasive tumors, verifying the results from the 3D-cultures. Gene expression profiling revealed enrichment of genes connected to translational control when either HSF1 or HSF2 was silenced. HSF1-specific targets were associated with progression of tumorigenesis, whereas HSF2 targets were involved in focal adhesion, critical for invasion. This study provides the first evidence for HSF2 functioning in cancer, i.e. as a tumor suppressor. Moreover, human PrCa tissue microarrays demonstrated increased nuclear HSF1 expression, which significantly correlated with high-grade Gleason score. Cytoplasmic HSF1 was detected in a subset of tumors and intriguingly, correlated with decreased disease-specific survival. This was most pronounced in intermediate Gleason score 7 tumors and in metastases. We propose the use of HSF1 as a biomarker to predict PrCa outcome, thus facilitating clinical decision-making and supporting individualized treatment choices. HSF1 and HSF2 siRNA transfection was performed in triplicates (biological replicates), for 5 and 8 days prior to harvesting total RNA; and compared to PC-3 cells transfected with scrambled control siRNAs for 5 and 8 days, respectively.
2013-12-23 | E-GEOD-48672 | biostudies-arrayexpress
Project description:Heat shock factor 1 (HSF1) is well known for its role in the heat shock response (HSR), where it drives a transcriptional program comprising heat shock protein (HSP) genes, and in tumorigenesis, where it drives a program comprising HSPs and many non-canonical target genes that support malignancy. Here, we find that HSF2, an HSF1 paralog with no significant role in the HSR, physically and functionally interacts with HSF1 across diverse types of cancer. HSF1 and HSF2 have strikingly similar chromatin occupancy and regulate a common set of genes which include both HSPs and non-canonical transcriptional targets with roles critical in supporting malignancy. Loss of either HSF1 or HSF2 results in a dysregulated response to nutrient stresses in vitro and reduced tumor progression in cancer cell line xenografts. Taken together, these findings establish HSF2 as a critical cofactor of HSF1 in driving a cancer cell transcriptional program to support the anabolic malignant state.
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Project description:Genome-wide characterization of binding sites for heat shock transcription factors HSF1 and HSF2 in freely cycling and mitotic K562 cells in optimal growth conditions and upon 30 min heat stress at 42C
2013-08-04 | GSE43579 | GEO
Project description:To analyze target genes of human heat shock transcription factor 1 (HSF1), we first generated two independent HeLa clones (RDT1 and RDT2) expressing an actively mutated hHSF1 (hHSF1ΔRDT), which lacks the regulatory domain that masks its activation domain and possesses a glutamic acid at amino acid 395 instead of a leucine in the suppression domain of the trimerization domain (Fujimoto et al., J. Biol. Chem. 280, 34908-34916, 2005). We also generated a HeLa clone expressing chicken HSF1 (HeLa/cHSF1) to compare its profile of gene expression with those of RDT1 and RDT2 cells (Nakai and Morimoto, Mol. Cell. Biol. 13, 1983-1997, 1993). We then carried out DNA microarray analysis using total RNA isolated from HeLa, HeLa/cHSF1, RDT1, and RDT2 cells grown under normal growth conditions.
2010-09-22 | GSE19797 | GEO
Project description:To analyze target genes of human heat shock transcription factor 1 (HSF1), we first generated two independent HeLa clones (RDT1 and RDT2) expressing an actively mutated hHSF1 (hHSF1?RDT), which lacks the regulatory domain that masks its activation domain and possesses a glutamic acid at amino acid 395 instead of a leucine in the suppression domain of the trimerization domain (Fujimoto et al., J. Biol. Chem. 280, 34908-34916, 2005). We also generated a HeLa clone expressing chicken HSF1 (HeLa/cHSF1) to compare its profile of gene expression with those of RDT1 and RDT2 cells (Nakai and Morimoto, Mol. Cell. Biol. 13, 1983-1997, 1993). We then carried out DNA microarray analysis using total RNA isolated from HeLa, HeLa/cHSF1, RDT1, and RDT2 cells grown under normal growth conditions. mRNA levels in human HeLa, RDT1, RDT2, and HeLa/cHSF1 were analyzed by DNA microarray analysis using GeneChip Human Genome U133 Plus 2.0 Array (Affymetrix).
2010-09-22 | E-GEOD-19797 | biostudies-arrayexpress
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
Project description:Mouse HSF1+/+ and HSF1-/- Fibroblasts Heat Shock Time Courses Scanned on Scanner 7 (Axon 4000B) Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set
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