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Article

The role of CDK1 in apoptin-induced apoptosis in hepatocellular carcinoma cells

  • Authors:
    • Jing Zhao
    • Su-Xia Han
    • Jin-Lu Ma
    • Xia Ying
    • Peijun Liu
    • Juan Li
    • Lijuan Wang
    • Ying Zhang
    • Jiguang Ma
    • Li Zhang
    • Qing Zhu
  • View Affiliations / Copyright

    Affiliations: Department of Oncology, The First Affiliated Hospital, Xi'an Jiaotong University Medical college, Xi'an, Shaanxi 710061, P.R. China, Center for Translational Medicine, The First Affiliated Hospital, Xi'an Jiaotong University Medical college, Xi'an, Shaanxi 710061, P.R. China
  • Pages: 253-259
    |
    Published online on: April 25, 2013
       https://doi.org/10.3892/or.2013.2426
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Abstract

Apoptin, a small protein derived from the chicken anemia virus, specifically induces apoptosis in transformed cells or tumor cells but not in normal cells. Thus, apoptin is involved in a general, tumor-specific pathway. Apoptin-induced apoptosis presumably requires additional interaction partners that activate specific signaling pathways in cancer cells. A number of molecules interact with apoptin and play an important role in the nuclear localization of apoptin or its tumor-selective cytotoxicity. Our data indicated that apoptin selectively kills HepG2 hepatocellular carcinoma (HCC) cells but has no effect on the normal liver cell line HL-7702. Analyses of human HCC tissue samples confirmed that CDK1 (cyclin-dependent kinase 1) activity was detected in primary malignancies but not in healthy paraneoplastic tissues. shRNA knockdown of CDK1 significantly reduced the tumor-specific killing effects of apoptin, suggesting that CDK1 plays an important role in the regulation of apoptin-induced apoptosis. Furthermore, the majority of apoptin translocated to the cytoplasm from the nucleus after knockdown of CDK1. Collectively, our results revealed for the first time that apoptin interacts with CDK1 in the complex process of tumorigenesis. The link between CDK1 and apoptin may be a novel cellular signaling pathway to modulate apoptosis in cancer; therefore, apoptin may have pharmacological potential to be directly employed for cancer therapy.
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Copy and paste a formatted citation
Spandidos Publications style
Zhao J, Han S, Ma J, Ying X, Liu P, Li J, Wang L, Zhang Y, Ma J, Zhang L, Zhang L, et al: The role of CDK1 in apoptin-induced apoptosis in hepatocellular carcinoma cells. Oncol Rep 30: 253-259, 2013.
APA
Zhao, J., Han, S., Ma, J., Ying, X., Liu, P., Li, J. ... Zhu, Q. (2013). The role of CDK1 in apoptin-induced apoptosis in hepatocellular carcinoma cells. Oncology Reports, 30, 253-259. https://doi.org/10.3892/or.2013.2426
MLA
Zhao, J., Han, S., Ma, J., Ying, X., Liu, P., Li, J., Wang, L., Zhang, Y., Ma, J., Zhang, L., Zhu, Q."The role of CDK1 in apoptin-induced apoptosis in hepatocellular carcinoma cells". Oncology Reports 30.1 (2013): 253-259.
Chicago
Zhao, J., Han, S., Ma, J., Ying, X., Liu, P., Li, J., Wang, L., Zhang, Y., Ma, J., Zhang, L., Zhu, Q."The role of CDK1 in apoptin-induced apoptosis in hepatocellular carcinoma cells". Oncology Reports 30, no. 1 (2013): 253-259. https://doi.org/10.3892/or.2013.2426
Copy and paste a formatted citation
x
Spandidos Publications style
Zhao J, Han S, Ma J, Ying X, Liu P, Li J, Wang L, Zhang Y, Ma J, Zhang L, Zhang L, et al: The role of CDK1 in apoptin-induced apoptosis in hepatocellular carcinoma cells. Oncol Rep 30: 253-259, 2013.
APA
Zhao, J., Han, S., Ma, J., Ying, X., Liu, P., Li, J. ... Zhu, Q. (2013). The role of CDK1 in apoptin-induced apoptosis in hepatocellular carcinoma cells. Oncology Reports, 30, 253-259. https://doi.org/10.3892/or.2013.2426
MLA
Zhao, J., Han, S., Ma, J., Ying, X., Liu, P., Li, J., Wang, L., Zhang, Y., Ma, J., Zhang, L., Zhu, Q."The role of CDK1 in apoptin-induced apoptosis in hepatocellular carcinoma cells". Oncology Reports 30.1 (2013): 253-259.
Chicago
Zhao, J., Han, S., Ma, J., Ying, X., Liu, P., Li, J., Wang, L., Zhang, Y., Ma, J., Zhang, L., Zhu, Q."The role of CDK1 in apoptin-induced apoptosis in hepatocellular carcinoma cells". Oncology Reports 30, no. 1 (2013): 253-259. https://doi.org/10.3892/or.2013.2426
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