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miR-539 inhibits FSCN1 expression and suppresses hepatocellular carcinoma migration and invasion

  • Authors:
    • Yanping Liu
    • Wei Hong
    • Cancan Zhou
    • Zhengdong Jiang
    • Guanghui Wang
    • Guangbing Wei
    • Xuqi Li
  • View Affiliations / Copyright

    Affiliations: Department of Vascular Surgery, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China, Department of General Surgery, Ankang City Central Hospital, Ankang, Shaanxi 725000, P.R. China, Department of Hepatobiliary Surgery, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China, Department of General Surgery, First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China
    Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 2593-2602
    |
    Published online on: April 3, 2017
       https://doi.org/10.3892/or.2017.5549
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Abstract

Increasing evidence indicates that the dysregulation of miRNAs that act as tumor suppressors or oncogenes is involved in tumorigenesis. However, the role of miR-539 in hepatocellular carcinoma (HCC) has not been well investigated. Quantitative RT-PCR (qRT-PCR), proliferation assay, colony formation assay, migration and invasion assays, western blotting, and xenograft tumor growth models were performed to assess the expression levels and functions of miR-539 in HCC. Luciferase reporter assays, qRT-PCR, western blotting, and immunohistochemistry were used to identify and verify the targets of miR-539. miR-539 was significantly downregulated in HCC cell lines and tissue samples. Ectopic expression of miR-539 inhibited cell viability, proliferation, migration, and invasion in vitro and suppressed xenograft tumor growth in vivo. Fascin homologue 1 (FSCN1) was verified as a direct target of miR-539, and overexpression of FSCN1 promoted HCC cell migration and invasion. miR-539 acts as a novel tumor suppressor in the development and progression of HCC by targeting FSCN1, providing new insight into the mechanisms of HCC carcinogenesis and suggesting that miR-539 may be a therapeutic target.
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Copy and paste a formatted citation
Spandidos Publications style
Liu Y, Hong W, Zhou C, Jiang Z, Wang G, Wei G and Li X: miR-539 inhibits FSCN1 expression and suppresses hepatocellular carcinoma migration and invasion. Oncol Rep 37: 2593-2602, 2017.
APA
Liu, Y., Hong, W., Zhou, C., Jiang, Z., Wang, G., Wei, G., & Li, X. (2017). miR-539 inhibits FSCN1 expression and suppresses hepatocellular carcinoma migration and invasion. Oncology Reports, 37, 2593-2602. https://doi.org/10.3892/or.2017.5549
MLA
Liu, Y., Hong, W., Zhou, C., Jiang, Z., Wang, G., Wei, G., Li, X."miR-539 inhibits FSCN1 expression and suppresses hepatocellular carcinoma migration and invasion". Oncology Reports 37.5 (2017): 2593-2602.
Chicago
Liu, Y., Hong, W., Zhou, C., Jiang, Z., Wang, G., Wei, G., Li, X."miR-539 inhibits FSCN1 expression and suppresses hepatocellular carcinoma migration and invasion". Oncology Reports 37, no. 5 (2017): 2593-2602. https://doi.org/10.3892/or.2017.5549
Copy and paste a formatted citation
x
Spandidos Publications style
Liu Y, Hong W, Zhou C, Jiang Z, Wang G, Wei G and Li X: miR-539 inhibits FSCN1 expression and suppresses hepatocellular carcinoma migration and invasion. Oncol Rep 37: 2593-2602, 2017.
APA
Liu, Y., Hong, W., Zhou, C., Jiang, Z., Wang, G., Wei, G., & Li, X. (2017). miR-539 inhibits FSCN1 expression and suppresses hepatocellular carcinoma migration and invasion. Oncology Reports, 37, 2593-2602. https://doi.org/10.3892/or.2017.5549
MLA
Liu, Y., Hong, W., Zhou, C., Jiang, Z., Wang, G., Wei, G., Li, X."miR-539 inhibits FSCN1 expression and suppresses hepatocellular carcinoma migration and invasion". Oncology Reports 37.5 (2017): 2593-2602.
Chicago
Liu, Y., Hong, W., Zhou, C., Jiang, Z., Wang, G., Wei, G., Li, X."miR-539 inhibits FSCN1 expression and suppresses hepatocellular carcinoma migration and invasion". Oncology Reports 37, no. 5 (2017): 2593-2602. https://doi.org/10.3892/or.2017.5549
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