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| BRCA2- and CDKN1A-interacting protein (BCCIP) has been considered an important cofactor for BRCA2 in tumor suppression. We previously observed the down-regulation of BCCIP in multiple clinically diagnosed primary tumor tissues including ovarian cancer, renal cell carcinoma and colorectal carcinoma. In this study, we first demonstrate that BCCIP expression was regulated by human INO80 (hINO80) chromatin remodeling complex in cells. In chromatin immunoprecipitation (ChIP) assays, we show that the catalytic subunit hINO80 protein and YY1, a subunit of hINO80 complex, co-localize the BCCIP promoter region (+0.25 kb downstream of the BCCIP), and the existence of hINO80 is required for recruiting the hINO80 complex to BCCIP promoter. RNAi knockdown of hINO80, Arp8 or YY1 resulted in reduction of BCCIP expression both in mRNA and protein level. In contrast, over-expression of hINO80, Arp8 or Arp5 enhanced the luciferase activity of pGL4-BCCIP. Together, as a novel target gene, BCCIP is regulated by hINO80 chromatin remodeling complex. Our findings will provide: 1) a theoretical basis to further elucidate the collaborative functions between the hINO80 complex and BCCIP in human cells; 2) an experimental basis for clarifying the role of BCCIP and BRCA2 in tumor suppression.
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| Keywords:BCCIP; INO80; chromatin remodeling complex |
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