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Increase in CIP2A expression is associated with doxorubicin resistance
Author(s) -
Choi Yeon A.,
Park Jeong Su,
Park Mi Young,
Oh Ki Sook,
Lee Myung Sok,
Lim Jong-Seok,
Kim Keun Il,
Kim Kun-yong,
Kwon Junhye,
Yoon Do Young,
Moon Eun-Yi,
Yang Young
Publication year - 2011
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2011.01.018
Subject(s) - doxorubicin , protein phosphatase 2 , mutant , cell growth , chemistry , cancer cell , phosphatase , cancer research , biology , microbiology and biotechnology , phosphorylation , chemotherapy , cancer , gene , biochemistry , genetics
The cancerous inhibitor of protein phosphatase 2A (CIP2A) increases the migration and metastasis of various cancer cells. Overexpression of CIP2A has been shown to increase the proliferation of MDA‐MB‐231 cells. We thus assessed whether CIP2A expression is associated with sensitivity to doxorubicin. MDA‐MB‐231 cells showed an increase in CIP2A expression after treatment with doxorubicin, while MCF‐7 cells showed a decrease in CIP2A expression. The overexpression of CIP2A in MCF‐7 cells overcame the inhibition of cell proliferation in response to doxorubicin treatment. CIP2A expression was not affected by wild‐type or mutant p53. However, mutant p53 blocked doxorubicin‐mediated CIP2A down‐regulation in HCT116 cells. As a regulation mechanism of doxorubicin‐mediated CIP2A expression, we showed that phosphorylated Akt was involved in the suppression of CIP2A expression.