Open AccessUbiquitination of p53 is Involved in Troglitazone Induced Apoptosis in Cervical Cancer Cells
Author(s) -
Huimin Chen,
Dingguo Zhang,
Jin-Xiz Wu,
DongSheng Pei,
Jian Zheng
Publication year - 2014
Publication title -
asian pacific journal of cancer prevention
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.512
H-Index - 75
eISSN - 2476-762X
pISSN - 1513-7368
DOI - 10.7314/apjcp.2014.15.5.2313
Subject(s) - troglitazone , apoptosis , peroxisome proliferator activated receptor , cell growth , cancer research , hela , annexin , cancer cell , biology , cell , chemistry , microbiology and biotechnology , receptor , cancer , biochemistry , genetics
Peroxisome proliferator-activated receptor gamma (PPAR-γ), a ligand-dependent nuclear transcription factor, has been found to widely exist in tumor tissues and plays an important role in affecting tumor cell growth. In this study, we investigated the effect of PPAR-γ on aspects of the cervical cancer malignant phenotype, such as cell proliferation and apoptosis. Cell growth assay, Western blotting, Annexin V and flow cytometry analysis consistently showed that treatment with troglitazone (TGZ, a PPAR-γ agonist) led to dose-dependent inhibition of cervical cancer cell growth through apoptosis, whereas T0070907 (another PPAR-γ antagonist???) had no effect on Hela cell proliferation and apoptosis. Furthermore, we also detected the protein expression of p53, p21 and Mdm2 to explain the underlying mechanism of PPAR-γ on cellular apoptosis. Our work, finally, demonstrated the existence of the TGZ-PPAR-γ-p53 signaling pathway to be a critical regulator of cell apoptosis. These results suggested that PPAR-γ may be a potential therapeutic target for cervical cancer.