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Article

PEG10 promotes human breast cancer cell proliferation, migration and invasion

  • Authors:
    • Xinran Li
    • Ruijing Xiao
    • Kingsley Tembo
    • Ling Hao
    • Meng Xiong
    • Shan Pan
    • Xiangyong Yang
    • Wen Yuan
    • Jie Xiong
    • Qiuping Zhang
  • View Affiliations / Copyright

    Affiliations: Department of Immunology, School of Basic Medical Sciences, Wuhan University, Wuhan, Hubei 430071, P.R. China, Hubei University of Technology Engineering and Technology College, Wuhan, Hubei 430068, P.R. China
  • Pages: 1933-1942
    |
    Published online on: February 23, 2016
       https://doi.org/10.3892/ijo.2016.3406
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Abstract

Paternally expressed imprinted gene 10 (PEG10), derived from the Ty3/Gypsy family of retrotransposons, has been implicated as a genetic imprinted gene. Accumulating evidence suggests that PEG10 plays an important role in tumor growth in various cancers, including hepatocellular carcinoma, lung cancer and prostate cancer. However, the correlation between PEG10 and breast cancer remains unclear. In the present study, we evaluated and characterized the role of PEG10 in human breast cancer proliferation, cell cycle, clone formation, migration and invasion. The expression level of PEG10 was significantly elevated in breast cancer tissues and associated with distant metastasis and poor clinical outcome. Gene set enrichment analysis indicated that high expression of PEG10 could enrich cell cycle-related processes in breast cancer tissues. Ectopic overexpression of PEG10 in breast cancer cells enhanced cell proliferation, cell cycle, clone formation along with migration and invasion. Cell-to-cell junction molecule E-cadherin was downregulated and matrix degradation proteases MMP-1, MMP-2, MMP-9 were up­regulated after PEG10 overexpression. Our results demonstrated that PEG10 is a crucial oncogene and has prognostic value for breast cancer, which could be applied in breast cancer diagnosis and targeting therapy in future.
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Copy and paste a formatted citation
Spandidos Publications style
Li X, Xiao R, Tembo K, Hao L, Xiong M, Pan S, Yang X, Yuan W, Xiong J, Zhang Q, Zhang Q, et al: PEG10 promotes human breast cancer cell proliferation, migration and invasion. Int J Oncol 48: 1933-1942, 2016.
APA
Li, X., Xiao, R., Tembo, K., Hao, L., Xiong, M., Pan, S. ... Zhang, Q. (2016). PEG10 promotes human breast cancer cell proliferation, migration and invasion. International Journal of Oncology, 48, 1933-1942. https://doi.org/10.3892/ijo.2016.3406
MLA
Li, X., Xiao, R., Tembo, K., Hao, L., Xiong, M., Pan, S., Yang, X., Yuan, W., Xiong, J., Zhang, Q."PEG10 promotes human breast cancer cell proliferation, migration and invasion". International Journal of Oncology 48.5 (2016): 1933-1942.
Chicago
Li, X., Xiao, R., Tembo, K., Hao, L., Xiong, M., Pan, S., Yang, X., Yuan, W., Xiong, J., Zhang, Q."PEG10 promotes human breast cancer cell proliferation, migration and invasion". International Journal of Oncology 48, no. 5 (2016): 1933-1942. https://doi.org/10.3892/ijo.2016.3406
Copy and paste a formatted citation
x
Spandidos Publications style
Li X, Xiao R, Tembo K, Hao L, Xiong M, Pan S, Yang X, Yuan W, Xiong J, Zhang Q, Zhang Q, et al: PEG10 promotes human breast cancer cell proliferation, migration and invasion. Int J Oncol 48: 1933-1942, 2016.
APA
Li, X., Xiao, R., Tembo, K., Hao, L., Xiong, M., Pan, S. ... Zhang, Q. (2016). PEG10 promotes human breast cancer cell proliferation, migration and invasion. International Journal of Oncology, 48, 1933-1942. https://doi.org/10.3892/ijo.2016.3406
MLA
Li, X., Xiao, R., Tembo, K., Hao, L., Xiong, M., Pan, S., Yang, X., Yuan, W., Xiong, J., Zhang, Q."PEG10 promotes human breast cancer cell proliferation, migration and invasion". International Journal of Oncology 48.5 (2016): 1933-1942.
Chicago
Li, X., Xiao, R., Tembo, K., Hao, L., Xiong, M., Pan, S., Yang, X., Yuan, W., Xiong, J., Zhang, Q."PEG10 promotes human breast cancer cell proliferation, migration and invasion". International Journal of Oncology 48, no. 5 (2016): 1933-1942. https://doi.org/10.3892/ijo.2016.3406
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