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Inactivated tumor suppressor Rb by nitric oxide promotes mitosis in human breast cancer cells
Author(s) -
Radisavljevic Ziv
Publication year - 2004
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.20063
Subject(s) - retinoblastoma protein , retinoblastoma , suppressor , phosphorylation , mitosis , cancer research , cell cycle , cell growth , tumor suppressor gene , cancer cell , chemistry , cancer , cell , nitric oxide , biology , microbiology and biotechnology , carcinogenesis , endocrinology , biochemistry , genetics , gene
Inactivation of tumor suppressor protein retinoblastoma (Rb) is important mechanism for the G 1 /S transition during cell cycle progression. Human breast cancer cells T47D release great amount of nitric oxide (NO), but its relation to tumor suppressor Rb is unknown. In this study, it is shown that NO induces phosphorylation and inactivation of Rb tumor suppressor protein, increasing G 2 /M phase and cell proliferation of breast cancer cells T47D. NO did not induce changes in p53 ser‐15 phosphorylation, the most phosphorylated site of p53 during its activation. These data indicate that NO induces cell proliferation through the Rb pathway. NO phosphorylates and inactivates tumor suppressor protein Rb inducing mitosis by the p53 independent pathway in breast cancer cell. © 2004 Wiley‐Liss, Inc.