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We analyzed the BCCIP protein level in 470 cases of human breast cancer to determine the associations between BCCIP and 53BP1, p53, and subtypes of breast cancer. We further constructed a unique BCCIP knockdown mouse model to determine whether a partial BCCIP deficiency leads to spontaneous breast cancer formation
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BCCIPbeta, as a S7 modulator, contributes to the regulation of ribosomal and extraribosomal functions of S7 and has implications in cell growth and tumor development.
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this study identifies BCCIP as a novel factor critical for microtubule regulation and explicates a mechanism utilized by BCCIP in tumor suppression.
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Expression of BCCIP beta was notably higher in tumor tissues of esophageal squamous cell carcinoma (ESCC) and Eca 109 cells. In vitro studies such as starvation and refeeding assay along with BCCIP beta-shRNA transfection assay demonstrated that BCCIP beta expression promoted proliferation of ESCC cells.
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we demonstrate that BCCIPbeta induces a conformational change within the RAD51 filament that promotes release of ADP to help maintain an active presynaptic filament. Our findings reveal a functional role for BCCIPbeta as a RAD51 accessory factor in HR.
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the existence of both INO80 and YY1 is required for recruiting the INO80/YY1 complex to BCCIP promoter region. Our findings strongly indicate that BCCIP is a potential target gene of the INO80/YY1 complex.
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The BCCIPbeta, but not BCCIPalpha, interacts with EIF6 and RPL23/UL14 and stabilizes the latter.
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Results indicate that BCCIP germ line mutations are unlikely to be a major contributor to familial breast/ovarian cancer risk in our population.
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In BRCA2, two novel frame shift mutations were identified as 5073-5074delCT and 6866delC.
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BRCA2 germline mutations appear to have a milder clinical phenotype when compared to non-BRCA2 mutations, since survival is higher among breast cancer patients carrying a BRCA2 mutation compared to sporadic breast cancers.
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Unique de novo mutation of BRCA2 has been identified in a woman with early onset breast cancer.
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Overexpression of BCCIP beta delays the G1 to S progression and results in an elevated p21 expression
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BCCIP is critical for BRCA2- and RAD51-dependent responses to DNA damage and homologous recombinational repair.
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BCCIP in maintaining the transactivation activity of wild type p53; down-regulation of BCCIP as a novel mechanism to impair the p53 function in cells harboring wild type p53
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suggest an essential role of BCCIP in the maintenance of genomic integrity
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BCCIP-dependent repair of double strand breaks by homologous recombination is an early RAD51 response to ionizing radiation-induced DNA damage.
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LYRIC/AEG-1 is a negative regulator of BCCIPalpha, promoting proteasomal degradation either through direct interaction, or potentially through an indirect mechanism involving downstream effects of the NF-kappaB signaling pathway.
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BCCIP is phosphorylated by the Src tyrosine kinase and dephosphorylated by the PTPmu tyrosine phosphatase; neurite outgrowth assays suggest that BCCIP and PTPmu are in a common signal transduction pathway.
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BCCIP protein expression was not detectable in approximately 45% of all astrocytic tumors.
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regulation of p21 intracellular distribution is a new mechanism for BCCIP to modulate p21 functions
