Open AccessPeroxisome proliferator-activated receptor-γ agonist-mediated inhibition of cell growth is independent of apoptosis in human epidermoid carcinoma A431 cells
Author(s) -
Qian Li,
Ying Peng,
PingJiao Chen,
MengLei Wang,
Can Cao,
Hui Xiong,
Jing Zhang,
MingHua Chen,
Xuebiao Peng,
Kang Zeng
Publication year - 2018
Publication title -
oncology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2018.8136
Subject(s) - a431 cells , epidermoid carcinoma , apoptosis , cancer research , cell cycle , oncogene , agonist , molecular medicine , peroxisome proliferator activated receptor , receptor , chemistry , biology , carcinoma , medicine , biochemistry
Evidence suggests that peroxisome proliferator activated receptor-γ (PPAR-γ) acts as a tumor suppressor in multiple types of cancer; however, the role of action of PPAR-γ on human epidermoid carcinoma is unclear. The present study investigated the effects of a PPAR-γ agonist, rosiglitazone, on human epidermoid carcinoma cell growth using the A431 cell line. The effects of rosiglitazone on cell viability and proliferation were evaluated with MTS and [ 3 H] thymidine incorporation assays. The effects of rosiglitazone on the cell cycle and apoptosis were analyzed by flow cytometry, and western blotting. It was identified that rosiglitazone inhibited A431 cell proliferation in a dose-dependent manner, increased the proportion of cells in the G1 phase, but did not affect apoptosis. Consistently, there was a significant decrease in the expression of cell proliferation-associated proteins, including cyclin D1, cyclin-dependent kinase (Cdk)2 and Cdk4 in A431 cells treated with rosiglitazone. This decrease was rescued by a selective antagonist of PPAR-γ or specific PPAR-γ small interfering RNAs. However, the ratio of B-cell lymphoma 2 (Bcl-2) to Bcl-2 associated X protein, which is associated with cell apoptosis, was not affected by these treatments. The data of the present study suggest that the PPAR-γ agonist rosiglitazone inhibits human epidermoid carcinoma cell growth through regulating the expression of the cell cycle-associated proteins, and that this effect is independent of apoptosis.