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IKKe coordinates invasion and metastasis

ABSTRACT: IKKe was identified previously as a breast cancer oncogene and was associated with poor clinical outcome in ovarian cancer. In order to elucidate functional roles of IKKe, we used microarray analysis to identify genes changed upon IKKe shRNA knockdown and compared with genes affected in ovarian cancers

ORGANISM(S): Homo sapiens

PROVIDER: GSE42320 | GEO | 2012/11/16

SECONDARY ACCESSION(S): PRJNA181022

REPOSITORIES: GEO

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IKKe coordinates invasion and metastasis

Project description:IKKe was identified previously as a breast cancer oncogene and was associated with poor clinical outcome in ovarian cancer. In order to elucidate functional roles of IKKe, we used microarray analysis to identify genes changed upon IKKe shRNA knockdown and compared with genes affected in ovarian cancers IKKe was knockdowned by 2 different IKKe shRNAs in Ovcar5 in 6 replicates and candidate downstream targets were selected if changed by both shRNAs

2012-11-16 | E-GEOD-42320 | biostudies-arrayexpress

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Transcription profiling of mouse wild type (wt) and Ikbke knockout (Ikke) embryonic fibroblasts (EF)

Project description:WT and Ikbke-/- EF cells were stimulated with recombinant interferon beta for 6 hours. Cells lacking IKKe kinase show a defect in a subset of interferon stimulated gene transcription Experiment Overall Design: WT and Ikbke cells were either stimulated and left untreated to compare their response to interferon.

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CTCF promotes epithelial ovarian cancer metastasis by broadly controlling the expression of metastasis-associated genes

Project description:CCCTC-binding factor (CTCF) is an 11 zinc fingers transcription factor that functions as both an oncogenic and tumor suppressor, depending on the cancer types, through epigenetic regulation. Epigenetic regulation including DNA methylation and histone modifications are critically involved in cancer metastasis. We then hypothesized that CTCF might play a vital role in epithelial ovarian cancer metastasis. Firstly, we found that CTCF expression was elevated in ovarian cancer tissues compared to non-tumor tissues. The elevated expression of CTCF predicts poor prognosis of ovarian cancer patients. Then, we revealed that CTCF knockdown significantly inhibited the migration, invasion and metastasis of ovarian cancer cells, although it had no effect on cell proliferation and tumor growth, which have been demonstrated with both in vitro and in vivo experiments. More importantly, we observed a higher CTCF expression in metastatic lesions than that in primary lesions from ovarian cancer patients. Mechanically, PCR array demonstrated that CTCF might regulate a series of metastasis associated genes, including CTBP1, SERPINE1 and SRC. Finally, we observed positive correlations between CTCF expression and those three genes in epithelial ovarian cancer specimens. In conclusion, this study demonstrates that CTCF is an oncogene in ovarian cancer to promote tumor metastasis through broadly controlling the expression of metastasis-associated genes. Our findings suggest CTCF could be a novel drug target to treat ovarian cancer by interfering with cancer cell metastasis.

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