Abstract
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.
Highlights
Ovarian carcinoma is the second most common and the most deadly malignancy of the female reproductive system[1]
To determine whether MAPinduced cytotoxicity was due to induction of apoptotic cell death in SKOV-3 cells, we examined the levels of the apoptosis-associated proteins Bcl-2, Bcl-2associated death promoter (Bad) and phospho-Bad by Western blot analysis
Ovarian cancer is chemosensitive, tumors eventually recur in two-thirds of patients, even after optimal surgical debulking followed by chemotherapy with platinum and taxane compounds
Summary
Ovarian carcinoma is the second most common and the most deadly malignancy of the female reproductive system[1]. The molecular mechanisms of ovarian oncogenesis are poorly understood. A previous study revealed that while postmenopausal estrogen replacement therapy using non-progestin regimens was a risk factor of carcinogenesis in ovarian cancer, hormone replacement therapy (HRT) with progestin did not in-. Crease the incidence of ovarian cancer[2]. The use of combination oral contraceptives (estrogen combined with progestin) is associated with a decrease in the incidence of ovarian cancer[3,4]. A high dose of progestin reduces the risk of ovarian cancer to a greater extent than low-dose progestin formulations in women[5], suggesting a protective effect of progesterone against ovarian carcinogenesis. The underlying mechanisms for the correlation between the use of progesterone and ovarian carcinogenesis remain unclear
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