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Transcriptome Analysis of Cbx7 Knockdown Effects in Ovarian Clear Cell Adenocarcinoma Cell Lines

ABSTRACT: Cbx7 knockdown resulted in increase of genes related with apoptosis and inflammation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE47146 | GEO | 2013/11/01

SECONDARY ACCESSION(S): PRJNA204205

REPOSITORIES: GEO

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Transcriptome Analysis of Cbx7 Knockdown Effects in Ovarian Clear Cell Adenocarcinoma Cell Lines

Project description:Cbx7 knockdown resulted in increase of genes related with apoptosis and inflammation. Expression microarray was performed using RNA extracted from 2 ovarian clear cell adenocarcinoma cell lines, namely, KOC-7C and TOV21G, either trancduced by Cbx7 siRNA or control.

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The RNF26/CBX7 axis modulates the TNF signaling pathway to promote cell proliferation and regulate sensitivity to TKIs in ccRCC

Project description:We performed CBX7 knockdown in renal cancer cells along with RNA sequencing. The expression profiling showed TNF signaling as a potential CBX7 target and the conditions were also verified in clinical samples.

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Discovery and Characterization of a Cellular Potent Positive Allosteric Modulator of the Polycomb Repressive Complex 1 Chromodomain, CBX7

Project description:Polycomb-directed repression of gene expression is frequently misregulated in human diseases. A quantitative and target-specific cellular assay was utilized to discover the first potent positive allosteric modulator (PAM) peptidomimetic, UNC4976, of nucleic acid binding by CBX7, a chromodomain methyl-lysine reader of Polycomb repressive complex 1. The PAM activity of UNC4976 resulted in enhanced efficacy across three orthogonal cellular assays by simultaneously antagonizing H3K27me3-specific recruitment of CBX7 to target genes while increasing non-specific binding to DNA and RNA. PAM activity thereby reequilibrates PRC1 away from H3K27me3 target regions. Together, our discovery and characterization of UNC4976 not only revealed the most cellularly potent PRC1-specific chemical probe to date, but also uncovers a potential mechanism of Polycomb regulation with implications for non-histone lysine methylated interaction partners.

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