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Article

AP-2α inhibits hepatocellular carcinoma cell growth and migration

  • Authors:
    • Wenhuan Huang
    • Cheng Chen
    • Zhongheng Liang
    • Junlu Qiu
    • Xinxin Li
    • Xiang Hu
    • Shuanglin Xiang
    • Xiaofeng Ding
    • Jian Zhang
  • View Affiliations / Copyright

    Affiliations: Key Laboratory of Protein Chemistry and Development Biology of State Education Ministry of China, College of Life Science, Hunan Normal University, Changsha, Hunan 410081, P.R. China
  • Pages: 1125-1134
    |
    Published online on: January 5, 2016
       https://doi.org/10.3892/ijo.2016.3318
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Abstract

Transcription factor AP-2α is involved in many types of human cancers, but its role in hepatocellular carcinogenesis is largely unknown. In this study, we found that expression of AP-2α was low in 40% of human hepatocellular cancers compared with adjacent normal tissues by immunohistochemical analysis. Moreover, AP-2α expression was low or absent in hepatocellular cancer cell lines (HepG2, Hep3B, SMMC-7721 and MHHC 97-H). Human liver cancer cell lines SMMC-7721 and Hep3B stably overexpressing AP-2α were established by lentiviral infection and puromycin screening, and the ectopic expression of AP-2α was able to inhibit hepatocellular cancer cell growth and proliferation by cell viability, MTT assay and liquid colony formation in vitro and in vivo. Furthermore, AP-2α overexpression decreased liver cancer cell migration and invasion as assessed by wound healing and Transwell assays, increasing the sensitivity of liver cancer cells to cisplatin analyzed by MTT assays. Also AP-2α overexpression suppressed the sphere formation and renewed the ability of cancer stem cells. Finally, we found that AP-2α is epigenetically modified and modulates the levels of phosphorylated extracellular signal-regulated protein kinase (ERK), β-catenin, p53, EMT, and CD133 expression in liver cancer cell lines. These results suggested that AP-2α expression is low in human hepatocellular cancers by regulating multiple signaling to affect hepatocellular cancer cell growth and migration. Therefore, AP-2α might represent a novel potential target in human hepatocellular cancer therapy.
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Copy and paste a formatted citation
Spandidos Publications style
Huang W, Chen C, Liang Z, Qiu J, Li X, Hu X, Xiang S, Ding X and Zhang J: AP-2α inhibits hepatocellular carcinoma cell growth and migration . Int J Oncol 48: 1125-1134, 2016.
APA
Huang, W., Chen, C., Liang, Z., Qiu, J., Li, X., Hu, X. ... Zhang, J. (2016). AP-2α inhibits hepatocellular carcinoma cell growth and migration . International Journal of Oncology, 48, 1125-1134. https://doi.org/10.3892/ijo.2016.3318
MLA
Huang, W., Chen, C., Liang, Z., Qiu, J., Li, X., Hu, X., Xiang, S., Ding, X., Zhang, J."AP-2α inhibits hepatocellular carcinoma cell growth and migration ". International Journal of Oncology 48.3 (2016): 1125-1134.
Chicago
Huang, W., Chen, C., Liang, Z., Qiu, J., Li, X., Hu, X., Xiang, S., Ding, X., Zhang, J."AP-2α inhibits hepatocellular carcinoma cell growth and migration ". International Journal of Oncology 48, no. 3 (2016): 1125-1134. https://doi.org/10.3892/ijo.2016.3318
Copy and paste a formatted citation
x
Spandidos Publications style
Huang W, Chen C, Liang Z, Qiu J, Li X, Hu X, Xiang S, Ding X and Zhang J: AP-2α inhibits hepatocellular carcinoma cell growth and migration . Int J Oncol 48: 1125-1134, 2016.
APA
Huang, W., Chen, C., Liang, Z., Qiu, J., Li, X., Hu, X. ... Zhang, J. (2016). AP-2α inhibits hepatocellular carcinoma cell growth and migration . International Journal of Oncology, 48, 1125-1134. https://doi.org/10.3892/ijo.2016.3318
MLA
Huang, W., Chen, C., Liang, Z., Qiu, J., Li, X., Hu, X., Xiang, S., Ding, X., Zhang, J."AP-2α inhibits hepatocellular carcinoma cell growth and migration ". International Journal of Oncology 48.3 (2016): 1125-1134.
Chicago
Huang, W., Chen, C., Liang, Z., Qiu, J., Li, X., Hu, X., Xiang, S., Ding, X., Zhang, J."AP-2α inhibits hepatocellular carcinoma cell growth and migration ". International Journal of Oncology 48, no. 3 (2016): 1125-1134. https://doi.org/10.3892/ijo.2016.3318
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