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Article

MicroRNA-33a promotes cell proliferation and inhibits apoptosis by targeting PPARα in human hepatocellular carcinoma

  • Authors:
    • Weiping Chang
    • Lei Zhang
    • Yao Xian
    • Zhaoxiang Yu
  • View Affiliations / Copyright

    Affiliations: Department of General Surgery, The First Affiliated Hospital of Xi'an Medical University, Xi'an, Shaanxi 710077, P.R. China, Department of Nutrition, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China
  • Pages: 2507-2514
    |
    Published online on: March 20, 2017
       https://doi.org/10.3892/etm.2017.4236
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Abstract

MicroRNA-33a (miR-33a) is dysregulated in a number of human cancers, where it functions as an oncogenic miRNA. However, the clinical significance of miR‑33a and its underlying molecular pathways regarding the progression of hepatocellular carcinoma (HCC) are currently unknown. In the present study, it was observed that the level of miR‑33a expression was significantly increased in HCC tissues, relative to adjacent non‑tumor tissues. Increased miR‑33a expression was significantly correlated with poor prognostic features of HCC, including larger tumor size, higher Edmondson-Steiner grading and higher tumor‑node-metastasis tumor stage. Furthermore, high levels of miR‑33a expression were associated with decreases in the 5-year overall survival rate and recurrence‑free survival of patients with HCC. In addition, functional experiments indicated that overexpression of miR‑33a led to increased proliferation and reduced apoptosis of the HCC cell line Huh7, while knockdown of miR‑33a decreased proliferation and induced apoptosis in the HCC cell line HepG2. Furthermore, peroxisome proliferator activated receptor alpha (PPARα) was identified as a direct target of miR-33a in HCC. Upregulation of miR‑33a was found to reduce the levels of PPARα expression in Huh7 cells, while inhibition of miR‑33a lead to a downregulation in PPARα expression in HepG2 cells. Collectively, these results suggest that miR-33a regulates the proliferation and apoptosis of HCC cells, and is a potential prognostic marker of HCC.
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Copy and paste a formatted citation
Spandidos Publications style
Chang W, Zhang L, Xian Y and Yu Z: MicroRNA-33a promotes cell proliferation and inhibits apoptosis by targeting PPARα in human hepatocellular carcinoma. Exp Ther Med 13: 2507-2514, 2017.
APA
Chang, W., Zhang, L., Xian, Y., & Yu, Z. (2017). MicroRNA-33a promotes cell proliferation and inhibits apoptosis by targeting PPARα in human hepatocellular carcinoma. Experimental and Therapeutic Medicine, 13, 2507-2514. https://doi.org/10.3892/etm.2017.4236
MLA
Chang, W., Zhang, L., Xian, Y., Yu, Z."MicroRNA-33a promotes cell proliferation and inhibits apoptosis by targeting PPARα in human hepatocellular carcinoma". Experimental and Therapeutic Medicine 13.5 (2017): 2507-2514.
Chicago
Chang, W., Zhang, L., Xian, Y., Yu, Z."MicroRNA-33a promotes cell proliferation and inhibits apoptosis by targeting PPARα in human hepatocellular carcinoma". Experimental and Therapeutic Medicine 13, no. 5 (2017): 2507-2514. https://doi.org/10.3892/etm.2017.4236
Copy and paste a formatted citation
x
Spandidos Publications style
Chang W, Zhang L, Xian Y and Yu Z: MicroRNA-33a promotes cell proliferation and inhibits apoptosis by targeting PPARα in human hepatocellular carcinoma. Exp Ther Med 13: 2507-2514, 2017.
APA
Chang, W., Zhang, L., Xian, Y., & Yu, Z. (2017). MicroRNA-33a promotes cell proliferation and inhibits apoptosis by targeting PPARα in human hepatocellular carcinoma. Experimental and Therapeutic Medicine, 13, 2507-2514. https://doi.org/10.3892/etm.2017.4236
MLA
Chang, W., Zhang, L., Xian, Y., Yu, Z."MicroRNA-33a promotes cell proliferation and inhibits apoptosis by targeting PPARα in human hepatocellular carcinoma". Experimental and Therapeutic Medicine 13.5 (2017): 2507-2514.
Chicago
Chang, W., Zhang, L., Xian, Y., Yu, Z."MicroRNA-33a promotes cell proliferation and inhibits apoptosis by targeting PPARα in human hepatocellular carcinoma". Experimental and Therapeutic Medicine 13, no. 5 (2017): 2507-2514. https://doi.org/10.3892/etm.2017.4236
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