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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
  • View Affiliations / Copyright

    Affiliations: Department of Hepatobiliary and Pancreatic Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China
    Copyright: © Jin et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 4767-4771
    |
    Published online on: August 8, 2017
       https://doi.org/10.3892/ol.2017.6731
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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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Copy and paste a formatted citation
Spandidos Publications style
Jin Z, Jia B, Fu Y, Tan L, Chen Q, Jiang P and Liu Y: Ligands of the peroxisome proliferator-activated receptor γ inhibit hepatocellular carcinoma cell proliferation. Oncol Lett 14: 4767-4771, 2017.
APA
Jin, Z., Jia, B., Fu, Y., Tan, L., Chen, Q., Jiang, P., & Liu, Y. (2017). Ligands of the peroxisome proliferator-activated receptor γ inhibit hepatocellular carcinoma cell proliferation. Oncology Letters, 14, 4767-4771. https://doi.org/10.3892/ol.2017.6731
MLA
Jin, Z., Jia, B., Fu, Y., Tan, L., Chen, Q., Jiang, P., Liu, Y."Ligands of the peroxisome proliferator-activated receptor γ inhibit hepatocellular carcinoma cell proliferation". Oncology Letters 14.4 (2017): 4767-4771.
Chicago
Jin, Z., Jia, B., Fu, Y., Tan, L., Chen, Q., Jiang, P., Liu, Y."Ligands of the peroxisome proliferator-activated receptor γ inhibit hepatocellular carcinoma cell proliferation". Oncology Letters 14, no. 4 (2017): 4767-4771. https://doi.org/10.3892/ol.2017.6731
Copy and paste a formatted citation
x
Spandidos Publications style
Jin Z, Jia B, Fu Y, Tan L, Chen Q, Jiang P and Liu Y: Ligands of the peroxisome proliferator-activated receptor γ inhibit hepatocellular carcinoma cell proliferation. Oncol Lett 14: 4767-4771, 2017.
APA
Jin, Z., Jia, B., Fu, Y., Tan, L., Chen, Q., Jiang, P., & Liu, Y. (2017). Ligands of the peroxisome proliferator-activated receptor γ inhibit hepatocellular carcinoma cell proliferation. Oncology Letters, 14, 4767-4771. https://doi.org/10.3892/ol.2017.6731
MLA
Jin, Z., Jia, B., Fu, Y., Tan, L., Chen, Q., Jiang, P., Liu, Y."Ligands of the peroxisome proliferator-activated receptor γ inhibit hepatocellular carcinoma cell proliferation". Oncology Letters 14.4 (2017): 4767-4771.
Chicago
Jin, Z., Jia, B., Fu, Y., Tan, L., Chen, Q., Jiang, P., Liu, Y."Ligands of the peroxisome proliferator-activated receptor γ inhibit hepatocellular carcinoma cell proliferation". Oncology Letters 14, no. 4 (2017): 4767-4771. https://doi.org/10.3892/ol.2017.6731
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