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Estrogen receptor α mediates proliferation of breast cancer MCF –7 cells via a p21/ PCNA / E 2 F 1‐dependent pathway
Author(s) -
Liao Xing–Hua,
Lu Da–Lin,
Wang Nan,
Liu Long–Yue,
Wang Yue,
Li Yan–Qi,
Yan Ting–Bao,
Sun Xue–Guang,
Hu Peng,
Zhang Tong–Cun
Publication year - 2014
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/febs.12658
Subject(s) - proliferating cell nuclear antigen , estrogen receptor , mcf 7 , cell growth , gene knockdown , cancer research , estrogen , cell cycle , cancer cell , estrogen receptor alpha , biology , chemistry , breast cancer , cell , microbiology and biotechnology , apoptosis , cancer , endocrinology , biochemistry , human breast , genetics
High expression of estrogen receptor α ( ER α) is associated with a poor prognosis that correlates closely with cellular proliferation in breast cancer. However, the exact molecular mechanism by which ER α controls breast cancer cell proliferation is not clear. Here we report that ER α regulates the cell cycle by suppressing p53/p21 and up‐regulating proliferating cell nuclear antigen ( PCNA ) and proliferation‐related K i–67 antigen ( K i–67) to promote proliferation of MCF –7 cells. In addition, 17–β–estradiol ( E 2) enhances ER α‐induced proliferation of MCF –7 cells by stimulating expression of PCNA and K i–67. Knockdown of ER α significantly affects PCNA / K i–67 and p53/p21 expression. Furthermore, ER α inhibits the transcriptional activity of p53/p21 in an estrogen response element‐dependent manner. More importantly, we provide new evidence that ER α mediates proliferation of MCF –7 cells by up‐regulating mi R –17 to silence the expression of p21. Thus, these data provide new insights into the underlying effect of ERα on breast cancer proliferation.