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Interaction of p14 ARF with Brca1 in cancer cell lines and primary breast cancer
Author(s) -
He Lizhi,
Fan Catherine,
Ning Xiaoming,
Feng Xinchang,
Liu Yun,
Chen Biao,
Tang Damu
Publication year - 2008
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/j.cellbi.2008.07.018
Subject(s) - du145 , ectopic expression , endogeny , cancer research , cancer cell , cell growth , chemistry , microbiology and biotechnology , cell , cell culture , biology , cancer , biochemistry , genetics , lncap
We report an association between p14 ARF and Brca1 in which both proteins co‐immunoprecipitate (co‐IP) in DU145 cells. The N‐terminal 64 residues of p14 ARF encoded by exon 1β are sufficient for this association. Inside the cell, ectopic p14 ARF co‐localizes with ectopic and endogenous Brca1 in A375 cells. Endogenous p14 ARF co‐localizes with endogenous Brca1 in DU145 cells but not in H1299 cells. Since p14 ARF interacts with B23 in the nucleolus, Brca1 co‐localizes with B23 in DU145 but not in H1299 cells. While ectopic ARF potently inhibited DU145 cell proliferation, it had no effect on the proliferation of H1299 cells, suggesting that the interaction between ARF and Brca1 contributes to ARF‐mediated tumor suppression. Consistent with this notion, ectopic p14 ARF modulates endogenous Brca1 expression in MCF7 breast cancer cells and p14 ARF co‐localizes with Brca1 in normal breast epithelial cells. This co‐localization is enhanced in primary breast cancer. Taken together, the results show that p14 ARF associates with Brca1, which may play a major role in tumor suppression.