Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Gene expression analysis in CITED2 knockdown MDA-MB-231 human breast cancer cells.

ABSTRACT: The goal of this experiment is to explore the mechanism behind CITED2 (a non-DNA binding transcriptional co-activator) metastatic action by comparing gene expression changes between shScramble and shCITED2-expressing MDA-MB-231 cells.

ORGANISM(S): Homo sapiens

SUBMITTER: Swaathi Jayaraman

PROVIDER: E-MTAB-4267 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

CITED2 Modulates Breast Cancer Metastatic Ability through Effects on IKKα.

Jayaraman Swaathi S Doucet Michele M Lau Wen Min WM Kominsky Scott L SL

Molecular cancer research : MCR 20160523 8

<h4>Unlabelled</h4>Previously, we identified the transcriptional coactivator CITED2 as a potential facilitator of bone metastasis using a murine mammary cancer model. Extending these studies to human breast cancer, it was observed that CITED2 mRNA expression was significantly elevated in patient specimens of metastatic breast cancer relative to primary tumors, with highest levels in metastasis to bone relative to non-bone sites. To further evaluate CITED2 functions in breast cancer metastasis, C ...[more]

PMID: 27216153

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Project description:Previously, we have identified the RUNX2 gene as hypomethylated and overexpressed in post-chemotherapy (CT) primary cultures derived from epithelial ovarian cancer (EOC) patients, when compared to primary cultures derived from matched primary (prior to CT) tumors. However, we found no differences in the RUNX2 methylation in primary EOC tumors and EOC omental metastases, suggesting that DNA methylation-based epigenetic mechanisms have no impact on RUNX2 expression in advanced (metastatic) stage of the disease. Moreover, RUNX2 displayed significantly higher expression not only in metastatic tissue, but also in high-grade primary tumors and even in low malignant potential tumors. Knockdown of the RUNX2 expression in EOC cells led to sharp decrease of cell proliferation and significantly inhibited EOC cell migration and invasion. Gene expression profiling and consecutive network and pathway analyses confirmed these findings, as various genes and pathways known previously to be implicated in ovarian tumorigenesis, including EOC tumor invasion and metastasis, were found to be downregulated upon RUNX2 suppression, while a number of pro-apoptotic genes and some EOC tumor suppressor genes were induced. Taken together, our data are indicative for a strong oncogenic potential of the RUNX2 gene in EOC progression and suggest that RUNX2 might be a novel EOC therapeutic target. Further studies are needed to more completely elucidate the functional implications of RUNX2 and other members of the RUNX gene family in ovarian tumorigenesis. To better understand the molecular mechanisms of RUNX2 gene action in ovarian cancer cells, we employed the Agilent Whole Human Genome microarrays, containing ~ 44,000 genes to identify global gene expression changes upon RUNX2 suppression in SKOV3 cells. We compared the gene expression of the previously selected clone shRNA- RUNX2-knockdown clone 3 (cl3) against the corresponding control clone. The microarray experiments were performed in duplicates, as two hybridizations were carried out for the RUNX2-suppressing cell clone against the corresponding control, using a fluorescent dye reversal (dye-swap) technique.

Dataset Information

Gene expression analysis in CITED2 knockdown MDA-MB-231 human breast cancer cells.

Publications

CITED2 Modulates Breast Cancer Metastatic Ability through Effects on IKKα.

Similar Datasets

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