Ligands of the peroxisome proliferator-activated receptor γ inhibit hepatocellular carcinoma cell proliferation

Jin,Zhe; Jia,Baoxing; Fu,Yu; Tan,Ludong; Chen,Qingmin; Jiang,Peiqiang; Liu,Yahui

doi:10.3892/ol.2017.6731

Ligands of the peroxisome proliferator-activated receptor γ inhibit hepatocellular carcinoma cell proliferation

Authors:
- Zhe Jin
- Baoxing Jia
- Yu Fu
- Ludong Tan
- Qingmin Chen
- Peiqiang Jiang
- Yahui Liu
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Affiliations: Department of Hepatobiliary and Pancreatic Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China
Published online on: August 8, 2017 https://doi.org/10.3892/ol.2017.6731
Pages: 4767-4771
Copyright: © Jin et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

This study was designed to investigate the regulatory role of the peroxisome proliferator-activated receptor γ (PPARγ) in the growth of hepatocellular carcinoma cells under the hypothesis that the levels of the phosphatase and tensin homologue deleted on chromosome 10 (PTEN) mRNA and the phosphorylated Akt (pAkt) protein would be affected by the presence of different receptor ligand concentrations. SMMC-7721 hepatocellular carcinoma cells were cultured in the presence of different concentrations of either 15-deoxyprostaglandin J2 (15-d-PGJ2) or pioglitazone and experiments were conducted in order to determine cell growth changes and measure levels of PTEN mRNA and pAkt protein. Our results after treatment with MTT showed the addition of ligands to the cultured cells inhibited their proliferation in a time- and dose-dependent manner. Also, flow cytometry after PI treatment showed the presence of ligands in the growth media could increase the proportion of G0/G1 phase cells, and decrease the proportion of S phase cells. Finally, the same cells exhibited increased levels of the PTEN mRNA by RT-PCR and pAkt protein by western blot analysis. Taken together, our results support the notion that PPARγ ligands can inhibit the proliferation of hepatocellular carcinoma cells in a time- and dose-dependent manner, and that this is at least in part due to the resulting upregulation of PTEN expression.

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