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Hepatitis B virus X protein promotes epithelial‑mesenchymal transition and metastasis in hepatocellular carcinoma cell line HCCLM3 by targeting HMGA2

  • Authors:
    • Yong Zha
    • Qian Yao
    • Jin‑Sheng Liu
    • Yuan‑Yuan Wang
    • Wei‑Ming Sun
  • View Affiliations / Copyright

    Affiliations: Department of Gastroenterological Surgery, The Third Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650118, P.R. China
    Copyright: © Zha et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 5709-5714
    |
    Published online on: August 23, 2018
       https://doi.org/10.3892/ol.2018.9359
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Abstract

Chronic hepatitis B virus (HBV) infection is a major risk factor for hepatocellular carcinoma (HCC), and HBV X protein (HBx) serves an essential role in the development of HCC. However, its mechanism remains to be elucidated. The aim of the present study was to investigate the role and mechanism of the HBx protein in the epithelial‑mesenchymal transition (EMT) and metastasis of HCC. The HCCLM3 cell line was transfected with a HBx‑expressing vector. The effects of HBx overexpression on proliferation, migration, invasion and EMT capacities of the HCCLM3 cell line were evaluated using MTT, migration and invasion assays, and western blotting, respectively. Furthermore, the impact of High mobility group AT‑hook 2 (HMGA2) knockdown on HBx‑mediated metastasis was investigated in the HCC cell line HCCLM3. The results demonstrated that HBx significantly upregulated HMGA2 expression, and enhanced the proliferation, EMT, invasion and migration in HCC cells. Furthermore, HMGA2 knockdown almost abolished HBx‑induced EMT and metastasis in HCC. The results of the present study suggest that HBx promotes the proliferation, EMT, invasion and migration of HCC cells by targeting HMGA2. HMGB2 may serve as a potential therapeutic target for HBV‑associated HCC.
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Copy and paste a formatted citation
Spandidos Publications style
Zha Y, Yao Q, Liu JS, Wang YY and Sun WM: Hepatitis B virus X protein promotes epithelial‑mesenchymal transition and metastasis in hepatocellular carcinoma cell line HCCLM3 by targeting HMGA2. Oncol Lett 16: 5709-5714, 2018.
APA
Zha, Y., Yao, Q., Liu, J., Wang, Y., & Sun, W. (2018). Hepatitis B virus X protein promotes epithelial‑mesenchymal transition and metastasis in hepatocellular carcinoma cell line HCCLM3 by targeting HMGA2. Oncology Letters, 16, 5709-5714. https://doi.org/10.3892/ol.2018.9359
MLA
Zha, Y., Yao, Q., Liu, J., Wang, Y., Sun, W."Hepatitis B virus X protein promotes epithelial‑mesenchymal transition and metastasis in hepatocellular carcinoma cell line HCCLM3 by targeting HMGA2". Oncology Letters 16.5 (2018): 5709-5714.
Chicago
Zha, Y., Yao, Q., Liu, J., Wang, Y., Sun, W."Hepatitis B virus X protein promotes epithelial‑mesenchymal transition and metastasis in hepatocellular carcinoma cell line HCCLM3 by targeting HMGA2". Oncology Letters 16, no. 5 (2018): 5709-5714. https://doi.org/10.3892/ol.2018.9359
Copy and paste a formatted citation
x
Spandidos Publications style
Zha Y, Yao Q, Liu JS, Wang YY and Sun WM: Hepatitis B virus X protein promotes epithelial‑mesenchymal transition and metastasis in hepatocellular carcinoma cell line HCCLM3 by targeting HMGA2. Oncol Lett 16: 5709-5714, 2018.
APA
Zha, Y., Yao, Q., Liu, J., Wang, Y., & Sun, W. (2018). Hepatitis B virus X protein promotes epithelial‑mesenchymal transition and metastasis in hepatocellular carcinoma cell line HCCLM3 by targeting HMGA2. Oncology Letters, 16, 5709-5714. https://doi.org/10.3892/ol.2018.9359
MLA
Zha, Y., Yao, Q., Liu, J., Wang, Y., Sun, W."Hepatitis B virus X protein promotes epithelial‑mesenchymal transition and metastasis in hepatocellular carcinoma cell line HCCLM3 by targeting HMGA2". Oncology Letters 16.5 (2018): 5709-5714.
Chicago
Zha, Y., Yao, Q., Liu, J., Wang, Y., Sun, W."Hepatitis B virus X protein promotes epithelial‑mesenchymal transition and metastasis in hepatocellular carcinoma cell line HCCLM3 by targeting HMGA2". Oncology Letters 16, no. 5 (2018): 5709-5714. https://doi.org/10.3892/ol.2018.9359
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