Medroxyprogestogen enhances apoptosis of SKOV-3 cells via inhibition of the PI3K/Akt signaling pathway
Author(s) -
Yan Li,
Yi Jiang,
Yicong Wan,
Zhang Lin,
Weiwei Tang,
Jingjing Ma,
Shan Wu,
Wenjun Cheng
Publication year - 2013
Publication title -
journal of biomedical research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.617
H-Index - 31
eISSN - 2352-4685
pISSN - 1674-8301
DOI - 10.7555/jbr.27.20120051
Subject(s) - protein kinase b , apoptosis , pi3k/akt/mtor pathway , phosphorylation , annexin , ly294002 , kinase , chemistry , phosphatidylinositol , microbiology and biotechnology , cancer research , signal transduction , biology , biochemistry
We sought to assess the effect of progestin on the apoptosis of epithelial ovarian cancer cell line SKOV-3 and via regulation of phosphorylation signaling in. Epithelial ovarian cancer cell line SKOV-3 was treated with medroxyprogestogen, phosphatidylinositol 3-kinase inhibitor LY294002 and vehicle control. Akt, phospho-Akt, Bcl-2 and phospho-Bad proteins were examined by immunoblotting assays. Medroxyprogestogen-induced apoptosis was assessed by MTT assays and Annexin V apoptosis assay. We found no significant difference in Akt and Bad expression in both the medroxyprogestogen groups and the control group. The levels of phospho-Akt, Bcl-2 and phospho-Bad were decreased in all the medroxyprogestogen groups and significantly decreased in the high dose mitogen-activated protein (MAP) group (10 µmol/L). Viability of SKOV-3 was reduced and apparent apoptosis of SKOV-3 cells was observed with increased doses of MAP. The findings suggest that medroxyprogestogen can induce SKOV-3 cell apoptosis by inhibiting Akt phosphorylation.
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