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The ERRalpha metabolic nuclear receptor controls growth of colon cancer cells

ABSTRACT: Estrogen-Related Receptor alpha (ERRÎ±) is a nuclear receptor that acts principally as a regulator of metabolism processes particularly in tissues subjected to high-energy demand. Besides its implication in energy metabolism and mitochondrial biogenesis, ERRÎ± was recently associated with tumorigenesis. Notably, increased expression of ERRÎ± was noted in different cancerous tissues as breast, ovary and colon. However, supplemental studies are required to better understand the role of ERRÎ± in colon carcinoma. We used microarrays to detail gene expression during ERRalpha knockdown in HCT116 cells and identified distinct classes of up and down-regulated genes. Triplicate of HCT116 cell line was infected witn shscrambled(shCTL) and shERRalpha lentivirus and used for RNA extraction and hybridization on Affymetrix microarrays.

ORGANISM(S): Homo sapiens

SUBMITTER: Julie Carrier

PROVIDER: E-GEOD-38690 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The ERRalpha metabolic nuclear receptor controls growth of colon cancer cells

Project description:Estrogen-Related Receptor alpha (ERRα) is a nuclear receptor that acts principally as a regulator of metabolism processes particularly in tissues subjected to high-energy demand. Besides its implication in energy metabolism and mitochondrial biogenesis, ERRα was recently associated with tumorigenesis. Notably, increased expression of ERRα was noted in different cancerous tissues as breast, ovary and colon. However, supplemental studies are required to better understand the role of ERRα in colon carcinoma. We used microarrays to detail gene expression during ERRalpha knockdown in HCT116 cells and identified distinct classes of up and down-regulated genes.

2013-06-06 | GSE38690 | GEO

ERRalpha mediates metabolic adaptations that drive lapatinib resistance in breast cancer (ERRalpha binding profiles in breast cancer cells by ChIP-seq)

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Human cystatin D (CST5) locates in the nucleus at sites of active transcription and regulates gene expression

Project description:Cystatin D (CST5) is an inhibitor of several proteases of the cathepsin family that inhibits cell proliferation, migration and invasion of colon carcinoma cells. Some of these effects are unrelated to its antiprotease activity. Here, we use genome-wide expression microarrays to show that cystatin D regulates gene expression (including that of genes encoding transcription factors such as RUNX1, RUNX2, or MEF2C) in HCT116 cells. HCT116 colon adenocarcinoma cell lines stably expressing cystatin D (HCT116-CST5 clone 9 and clone 20), mock-transfected (HCT116-Mock) and un-transfected (HCT116-Untransfected) were generated as described (Ãlvarez-DÃaz et al., 2009, PUBMED:19662683) and genome-wide expression microarrays were obtained to achieve the gene expression profile induced by CST5.

2015-11-04 | E-GEOD-45904 | biostudies-arrayexpress

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ERRalpha mediates metabolic adaptations that drive lapatinib resistance in breast cancer (ERRalpha binding profiles in breast cancer cells by ChIP-seq)

2016-06-15 | E-GEOD-81651 | biostudies-arrayexpress

Human colon carcinoma cell line treated with bafilomycin A1

Project description:Analysis of mRNA expression changes in human colon carcinoma cell lines (HCT116 H2B-GFP) after treatment bafilomycin A1. mRNA expression analysis of HCT116 H2B-GFP treated with bafilomycin A1 compared to untreated HCT116 H2B-GFP. Four biological replicates were performed for treated samples.

2014-02-19 | E-GEOD-47836 | biostudies-arrayexpress

Functional Annotation of Colon Cancer Risk SNPs

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