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Article

MicroRNA-101 suppresses migration and invasion via targeting vascular endothelial growth factor-C in hepatocellular carcinoma cells

  • Authors:
    • Zhenyu Liu
    • Jingjie Wang
    • Yuqing Mao
    • Bing Zou
    • Xiaoming Fan
  • View Affiliations / Copyright

    Affiliations: Department of Gastroenterology and Hepatology, Jinshan Hospital, Fudan University, Shanghai 201508, P.R. China, Department of Gastroenterology and Hepatology, Shenzhen Hospital, Peking University, Shenzhen, Guangdong 518036, P.R. China
  • Pages: 433-438
    |
    Published online on: October 27, 2015
       https://doi.org/10.3892/ol.2015.3832
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Abstract

MicroRNAs (miRNAs) are a class of non‑coding RNAs 18-25 nucleotides in length, which play important roles in the regulation of cancer progression through gene silencing. miRNA (miR)‑101 has been suggested to be associated with hepatocellular carcinoma (HCC). However, the detailed role of miR‑101 in HCC metastasis and the underlying mechanism remain largely unclear. The present study demonstrated that the expression of miR‑101 was significantly reduced in HCC tissues compared with that in matched normal adjacent tissues. miR‑101 was also found to be downregulated in four HCC cell lines compared with its expression in a normal liver cell line. Vascular endothelial growth factor (VEGF)‑C was further identified as a direct target of miR‑101, and the protein expression of VEGF‑C was downregulated by miR‑101 in HepG2 HCC cells. Furthermore, the overexpression of miR‑101 and the knockdown of VEGF‑C significantly inhibited HepG2 cell migration and invasion, while restoration of VEGF‑C reversed the inhibitory effect of miR‑101 overexpression on HepG2 cell migration and invasion. Finally, the expression of VEGF‑C was notably increased in HCC tissues and cell lines. These findings suggest that miR‑101 exerts a suppressive effect on HCC cell migration and invasion, at least in part through the direct inhibition of VEGF‑C protein expression. Therefore, the miR‑101/VEGF‑C axis may serve as a potential therapeutic target for HCC metastasis.
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Copy and paste a formatted citation
Spandidos Publications style
Liu Z, Wang J, Mao Y, Zou B and Fan X: MicroRNA-101 suppresses migration and invasion via targeting vascular endothelial growth factor-C in hepatocellular carcinoma cells. Oncol Lett 11: 433-438, 2016.
APA
Liu, Z., Wang, J., Mao, Y., Zou, B., & Fan, X. (2016). MicroRNA-101 suppresses migration and invasion via targeting vascular endothelial growth factor-C in hepatocellular carcinoma cells. Oncology Letters, 11, 433-438. https://doi.org/10.3892/ol.2015.3832
MLA
Liu, Z., Wang, J., Mao, Y., Zou, B., Fan, X."MicroRNA-101 suppresses migration and invasion via targeting vascular endothelial growth factor-C in hepatocellular carcinoma cells". Oncology Letters 11.1 (2016): 433-438.
Chicago
Liu, Z., Wang, J., Mao, Y., Zou, B., Fan, X."MicroRNA-101 suppresses migration and invasion via targeting vascular endothelial growth factor-C in hepatocellular carcinoma cells". Oncology Letters 11, no. 1 (2016): 433-438. https://doi.org/10.3892/ol.2015.3832
Copy and paste a formatted citation
x
Spandidos Publications style
Liu Z, Wang J, Mao Y, Zou B and Fan X: MicroRNA-101 suppresses migration and invasion via targeting vascular endothelial growth factor-C in hepatocellular carcinoma cells. Oncol Lett 11: 433-438, 2016.
APA
Liu, Z., Wang, J., Mao, Y., Zou, B., & Fan, X. (2016). MicroRNA-101 suppresses migration and invasion via targeting vascular endothelial growth factor-C in hepatocellular carcinoma cells. Oncology Letters, 11, 433-438. https://doi.org/10.3892/ol.2015.3832
MLA
Liu, Z., Wang, J., Mao, Y., Zou, B., Fan, X."MicroRNA-101 suppresses migration and invasion via targeting vascular endothelial growth factor-C in hepatocellular carcinoma cells". Oncology Letters 11.1 (2016): 433-438.
Chicago
Liu, Z., Wang, J., Mao, Y., Zou, B., Fan, X."MicroRNA-101 suppresses migration and invasion via targeting vascular endothelial growth factor-C in hepatocellular carcinoma cells". Oncology Letters 11, no. 1 (2016): 433-438. https://doi.org/10.3892/ol.2015.3832
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