Peroxisome proliferator–activated receptor‐γ agonists cause growth arrest and apoptosis in human ovarian carcinoma cell lines

Peroxisome proliferator–activated receptor gamma (PPARγ) is a member of the nuclear hormone receptor superfamily of ligand‐activated transcription factors. PPARγ agonists inhibit the growth of many types of cancers. To our knowledge, the effect of PPARγ agonist on ovarian tumors is not reported. In this study, we used two human ovarian carcinoma cell lines (ES‐2 and PA‐1) to examine the effects of the PPARγ agonists troglitazone (TGZ) and ciglitazone (CGZ) on cell survival. CGZ and TGZ inhibited viability in a dose‐dependent manner in both types of ovarian cancer cells. The agonists also decreased cellular proliferation in association with an increase in the number of cells arrested in the G0/G1 phase of the cell cycle. Moreover, they increased apoptosis while increasing caspase‐3 activity. Incubation of both the cell lines with the PPARγ agonists led to upregulated PPARγ expression. This effect appeared to be PPARγ independent because the PPARγ antagonist GW9662 did not reverse it. Along with the induction of apoptosis in ovarian cancer cells, protein expression levels of p53 and Bax markedly increased in response to the PPARγ agonists. Our results demonstrated that PPARγ agonists inhibited the viability of human ovarian cancer cells, at least partly by inducing apoptosis. As a result, these agonists may serve as future drugs for the prevention and treatment of ovarian cancer.