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Gene expression changes after Ctcfl overexpression in undifferentiated and differentiated p19 cells.

ABSTRACT: The two paralogous zinc finger factors CTCF and CTCFL differ in expression such that CTCF is ubiquitously expressed, whereas CTCFL is found during spermatogenesis and in some cancer types. Both factors share the highly conserved DNA binding domain and are bound to DNA sequences with an identical consensus. Here we analyzed the differential gene expression effect mediated by expression of Ctcfl in undifferentiated and differentiated p19 cell.

ORGANISM(S): Mus musculus

PROVIDER: GSE103197 | GEO | 2018/05/30

REPOSITORIES: GEO

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Mapping of CTCF and CTCFL binding sites in 3T3 and p19 cells

Project description:Study of the differential binding behavior of the paralogous factors CTCF and CTCFL by ChIP-seq in mouse NIH3T3 and p19 cells.

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Gene expression changes after Ctcfl overexpression in NIH3T3 cells.

Project description:The two paralogous zinc finger factors CTCF and CTCFL differ in expression such that CTCF is ubiquitously expressed, whereas CTCFL is found during spermatogenesis and in some cancer types. Both factors share the highly conserved DNA binding domain and are bound to DNA sequences with an identical consensus. Here we analyzed the differential gene expression effect mediated by expression of Ctcfl in undifferentiated and differentiated NIH3T3 cell.

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Nucleosome dynamics specifies genome-wide binding of the male germ cell gene regulator CTCFL and of CTCF [ChIP-Seq]

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Project description:High-grade serous ovarian carcinoma (HGSC) is the most lethal gynecologic malignancy due to the lack of reliable biomarkers, effective treatment and chemoresistance. Improving the diagnosis and the development of targeted therapies is still needed. The molecular pathomechanisms driving HGSC progression are not fully understood though crucial for effective diagnosis and identification of novel targeted therapy options. The oncogene CTCFL (BORIS), the paralog of CTCF, is a transcriptional factor highly expressed in ovarian cancer (but in rarely any other tissue in females) with cancer-specific characteristics and therapeutic potential. In this work, we seek to understand the regulatory functions of CTCFL to unravel new target genes with clinical relevance. We used in vitro models to evaluate the transcriptional changes due to the presence of CTCFL, followed by a selection of gene candidates using de novo network enrichment analysis. The resulting mechanistic candidates were further assessed regarding their prognostic potential and druggability. We show that CTCFL-driven genes are involved in cytoplasmic membrane functions; in particular, the Pi3K-AKT initiators EGFR1 and VEGFA, as well as ITGB3 and ITGB6 are potential drug targets. Finally, we identified the CTCFL targets ACTBL2, MALT1 and PCDH7 as mechanistic biomarkers to predict survival in HGSC. Finally, we elucidated the value of CTCFL in combination with its targets as a prognostic marker profile for HGSC progression and as putative drug targets.

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