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HSF1 drives a transcriptional program distinct from heat shock to support highly malignant human cancers

ABSTRACT: This SuperSeries is composed of the following subset Series: GSE38232: HSF1 drives a transcriptional program distinct from heat shock to support highly malignant human cancers [gene expression] GSE38901: HSF1 drives a transcriptional program distinct from heat shock to support highly malignant human cancers [ChIP-Seq] Refer to individual Series

ORGANISM(S): Homo sapiens

SUBMITTER: Marc Mendillo

PROVIDER: E-GEOD-38912 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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HSF1 drives a transcriptional program distinct from heat shock to support highly malignant human cancers.

Mendillo Marc L ML Santagata Sandro S Koeva Martina M Bell George W GW Hu Rong R Tamimi Rulla M RM Fraenkel Ernest E Ince Tan A TA Whitesell Luke L Lindquist Susan S

Cell 20120801 3

Heat-Shock Factor 1 (HSF1), master regulator of the heat-shock response, facilitates malignant transformation, cancer cell survival, and proliferation in model systems. The common assumption is that these effects are mediated through regulation of heat-shock protein (HSP) expression. However, the transcriptional network that HSF1 coordinates directly in malignancy and its relationship to the heat-shock response have never been defined. By comparing cells with high and low malignant potential alo ...[more]

PMID: 22863008

Similar Datasets

HSF1 drives a transcriptional program distinct from heat shock to support highly malignant human cancers [ChIP-Seq]

Project description:Heat-Shock Factor 1 (HSF1), master regulator of the heat-shock response, facilitates malignant transformation, cancer cell survival and proliferation in model systems. The common assumption is that these effects are mediated through regulation of heat-shock protein (HSP) expression. However, the transcriptional network that HSF1 coordinates directly in malignancy and its relationship to the heat-shock response have never been defined. By comparing cells with high and low malignant potential alongside their non-transformed counterparts, we identify an HSF1-regulated transcriptional program specific to highly malignant cells and distinct from heat shock. Cancer-specific genes in this program support oncogenic processes: cell-cycle regulation, signaling, metabolism, adhesion and translation. HSP genes are integral to this program, however, even these genes are uniquely regulated in malignancy. This HSF1 cancer program is active in breast, colon and lung tumors isolated directly from human patients and is strongly associated with metastasis and death. Thus, HSF1 rewires the transcriptome in tumorigenesis, with prognostic and therapeutic implications. ChIP-seq was used to characterize HSF1 binding

2012-08-07 | E-GEOD-38901 | biostudies-arrayexpress

Tight coordination of protein translation and heat shock factor 1 activation supports the anabolic malignant state [ChIP-Seq]

Project description:A unifying characteristic of aggressive cancers is a profound anabolic shift in metabolism to enable sustained proliferation and biomass expansion. The ribosome is centrally situated to sense metabolic states but whether it impacts systems that promote cellular survival is unknown. Here, through integrated chemical-genetic analyses, we find that a dominant transcriptional effect of blocking protein translation in cancer cells is complete inactivation of heat shock factor 1 (HSF1), a multifaceted transcriptional regulator of the heat-shock response and many other cellular processes essential for tumorigenesis. Translational flux through the ribosome reshapes the transcriptional landscape and links the fundamental anabolic processes of protein production and energy metabolism with HSF1 activity. Targeting this link deprives cancer cells of their energy and chaperone armamentarium thereby rendering the malignant phenotype unsustainable. We used ChIP-Seq to examine affect of rocaglates and cycloheximide on HSF1 genomic occupancy in MCF7 and M0-91 cancer cells.

2013-07-21 | E-GEOD-45852 | biostudies-arrayexpress

Promoter proximal pausing and its regulation by c-Myc in embryonic stem cells: ChIP-Seq

Project description:Recruitment of the RNA Polymerase II (Pol II) transcription initiation apparatus to promoters by specific DNA binding transcription factors is well recognized as a key regulatory step in gene expression. We describe here evidence that promoter-proximal pausing is a general feature of transcription by Pol II in embryonic stem (ES) cells, and thus an additional step where regulation of gene expression may occur. We report here that c-Myc, which occupies a third of actively transcribed genes in ES cells and is a key regulator of cellular proliferation, binds P-TEFb and contributes to release of promoter-proximal paused Pol II at these genes. ChIP-seq data for Pol II and additional factors controlling pause release in mouse ES cells.

2010-04-02 | E-GEOD-20530 | biostudies-arrayexpress

Promoter proximal pausing and its regulation by c-Myc in embryonic stem cells

Project description:This SuperSeries is composed of the following subset Series: GSE20529: Promoter proximal pausing and its regulation by c-Myc in embryonic stem cells: ChIP-chip GSE20530: Promoter proximal pausing and its regulation by c-Myc in embryonic stem cells: ChIP-Seq Refer to individual Series

2010-04-14 | E-GEOD-20485 | biostudies-arrayexpress

HSF1 drives a transcriptional program distinct from heat shock to support highly malignant human cancers [gene expression]

2012-08-06 | E-GEOD-38232 | biostudies-arrayexpress

Tight coordination of protein translation and heat shock factor 1 activation supports the anabolic malignant state [Gene Expression Data]

Project description:A unifying characteristic of aggressive cancers is a profound anabolic shift in metabolism to enable sustained proliferation and biomass expansion. The ribosome is centrally situated to sense metabolic states but whether it impacts systems that promote cellular survival is unknown. Here, through integrated chemical-genetic analyses, we find that a dominant transcriptional effect of blocking protein translation in cancer cells is complete inactivation of heat shock factor 1 (HSF1), a multifaceted transcriptional regulator of the heat-shock response and many other cellular processes essential for tumorigenesis. Translational flux through the ribosome reshapes the transcriptional landscape and links the fundamental anabolic processes of protein production and energy metabolism with HSF1 activity. Targeting this link deprives cancer cells of their energy and chaperone armamentarium thereby rendering the malignant phenotype unsustainable. Gene Expression Data We used microarrays to examine affect of rocaglates on gene expression in cancer cell lines. MCF7 breast cancer cells were treated with either 200 nM Rocaglamide A or DMSO, as a control. Two biological replicates for all samples.

2013-07-21 | E-GEOD-45851 | biostudies-arrayexpress

ChIP-seq analysis of histone modifications and RNA polymerase II at 4 stages of directed cardiac differentiation of mouse embryonic stem cells

Project description:We interrogated the genome-wide occupancy of histone modifications and RNA polymerase II at several stages of an mouse embryonic stem cell to cardiomyocyte directed differentiation protocol. These four stages represent timepoints when differentiating cultures are enriched for embryonic stem cells (ESC), mesodermal cells (MES), cardiac precursors (CP), or cardiomyocytes (CM) respectively. This study revealed many dynamic patterns of histone modifications during differentiation that are coordinated with stage-specific gene expression including a novel preactivation chromatin pattern found at genes associated with cardiac function. In addition, this study identified distal enhancer elements and enriched transcription factor motifs within enhancer regions for each stage of differentiation, which were used to predict novel transcription regulatory networks. ChIP-seq analysis of histone modifications and RNA polymerase II at 4 stages of directed cardiac differentiation of mouse embryonic stem cells. Each stage in biological duplicate or triplicate

2013-06-15 | E-GEOD-47949 | biostudies-arrayexpress

Tight coordination of protein translation and heat shock factor 1 activation supports the anabolic malignant state

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-07-21 | E-GEOD-45853 | biostudies-arrayexpress

ChIP-Seq of Sox2 and Brn2 in ESCs, NPCs, and differentiating ESCs

Project description:We analyzed the genome-wide binding of Sox2 and POU factor partner factors, Oct4 in ESCs (using published datasets PMID:18692474 and GSM307137, GSM307154, GSM307155) and Brn2 in NPCs. We found that Sox2 and Oct4 co-occupied a large subset of promoters and enhancers in ESCs, but that Sox2 and Brn2 co-occupy predominantly enhancers. Further, we overexpressed Brn2 in differentiating ESCs and showed that ectopic Brn2 recruited Sox2 to NPC-specific targets, resulting in skewed differentiation towards the neural lineage. Examination of transcription factor binding in ESCs, NPCs, and differentiating ESCs by ChIP-Seq.

2013-02-20 | E-GEOD-35496 | biostudies-arrayexpress

Myc and SAGA Rewire an Alternative Splicing Network During Early Somatic Cell Reprogramming [Reprogramming_ChIPSEQ]

Project description:Embryonic stem cells are maintained in a self-renewing and pluripotent state by multiple regulatory pathways. Pluripotent-specific transcriptional networks are sequentially reactivated as somatic cells reprogram to achieve pluripotency. How epigenetic regulators modulate this process and contribute to somatic cell reprogramming is not clear. Here we perform a functional RNAi screen to identify the earliest epigenetic regulators required for reprogramming. We identify components of the SAGA histone acetyltransferase complex, in particular Gcn5, as critical regulators of reprogramming initiation. Furthermore, we show in mouse pluripotent stem cells that Gcn5 strongly associates with Myc and that upon initiation of somatic reprogramming, Gcn5 and Myc form a positive feed forward loop that activates a distinct alternative splicing network and the early acquisition of pluripotency-associated splicing events. These studies expose a Myc-SAGA pathway that drives expression of an essential alternative splicing regulatory network during somatic cell reprogramming. Examination of Myc-chromatin interactions in reprogramming cells

2015-04-15 | E-GEOD-67694 | biostudies-arrayexpress

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