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Article

Pien Tze Huang inhibits the growth of hepatocellular carcinoma cells by upregulating miR‑16 expression

  • Authors:
    • Fei Qi
    • Songqiang Zhou
    • Li Li
    • Lihui Wei
    • Aling Shen
    • Liya Liu
    • Yaodong Wang
    • Jun Peng
  • View Affiliations / Copyright

    Affiliations: Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China, Department of Hepatobiliary Surgery, Fujian Provincial Hospital, Fujian Medical University, Fuzhou, Fujian 350001, P.R. China, Department of Disease Prevention and Healthcare, Fujian Provincial Hospital, Fujian Medical University, Fuzhou, Fujian 350001, P.R. China
  • Pages: 8132-8137
    |
    Published online on: October 20, 2017
       https://doi.org/10.3892/ol.2017.7240
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Abstract

Hepatocellular carcinoma (HCC) is characterized by uncontrolled proliferation and the deregulation of apoptotic signaling, although its molecular pathogenesis is not fully characterized. The ability to inhibit excessive proliferation and induce the apoptosis of cancer cells are crucial characteristics of anticancer drugs. Pien Tze Huang (PZH) is a widely used traditional Chinese medicine for the treatment of various types of cancer, and has exhibited promising therapeutic effects in clinical trials of HCC. However, the underlying mechanisms for its action are unclear. In the present study, the aim was to explore the effect of PZH on the proliferation and apoptosis of the BEL‑7402 HCC cell line, and the associated mechanisms. PZH treatment significantly inhibited BEL‑7402 cell viability, confluence and clonogenicity, inducing cell cycle arrest and promoting apoptosis. In addition, PZH treatment suppressed the expression of the pro‑proliferative genes cyclin D1 and cyclin‑dependent kinase 4, and decreased the expression of the anti‑apoptotic gene Bcl‑2. PZH treatment also upregulated the expression of a key microRNA (miR), miR‑16. The study demonstrated that PZH can effectively inhibit cancer cell proliferation and induce apoptosis in BEL‑7402 HCC cells via the upregulation of the tumor suppressor miR‑16.
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Copy and paste a formatted citation
Spandidos Publications style
Qi F, Zhou S, Li L, Wei L, Shen A, Liu L, Wang Y and Peng J: Pien Tze Huang inhibits the growth of hepatocellular carcinoma cells by upregulating miR‑16 expression. Oncol Lett 14: 8132-8137, 2017.
APA
Qi, F., Zhou, S., Li, L., Wei, L., Shen, A., Liu, L. ... Peng, J. (2017). Pien Tze Huang inhibits the growth of hepatocellular carcinoma cells by upregulating miR‑16 expression. Oncology Letters, 14, 8132-8137. https://doi.org/10.3892/ol.2017.7240
MLA
Qi, F., Zhou, S., Li, L., Wei, L., Shen, A., Liu, L., Wang, Y., Peng, J."Pien Tze Huang inhibits the growth of hepatocellular carcinoma cells by upregulating miR‑16 expression". Oncology Letters 14.6 (2017): 8132-8137.
Chicago
Qi, F., Zhou, S., Li, L., Wei, L., Shen, A., Liu, L., Wang, Y., Peng, J."Pien Tze Huang inhibits the growth of hepatocellular carcinoma cells by upregulating miR‑16 expression". Oncology Letters 14, no. 6 (2017): 8132-8137. https://doi.org/10.3892/ol.2017.7240
Copy and paste a formatted citation
x
Spandidos Publications style
Qi F, Zhou S, Li L, Wei L, Shen A, Liu L, Wang Y and Peng J: Pien Tze Huang inhibits the growth of hepatocellular carcinoma cells by upregulating miR‑16 expression. Oncol Lett 14: 8132-8137, 2017.
APA
Qi, F., Zhou, S., Li, L., Wei, L., Shen, A., Liu, L. ... Peng, J. (2017). Pien Tze Huang inhibits the growth of hepatocellular carcinoma cells by upregulating miR‑16 expression. Oncology Letters, 14, 8132-8137. https://doi.org/10.3892/ol.2017.7240
MLA
Qi, F., Zhou, S., Li, L., Wei, L., Shen, A., Liu, L., Wang, Y., Peng, J."Pien Tze Huang inhibits the growth of hepatocellular carcinoma cells by upregulating miR‑16 expression". Oncology Letters 14.6 (2017): 8132-8137.
Chicago
Qi, F., Zhou, S., Li, L., Wei, L., Shen, A., Liu, L., Wang, Y., Peng, J."Pien Tze Huang inhibits the growth of hepatocellular carcinoma cells by upregulating miR‑16 expression". Oncology Letters 14, no. 6 (2017): 8132-8137. https://doi.org/10.3892/ol.2017.7240
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