Involvement of CD147 isoform‑4 in the proliferation of SiHa cells: A possible molecular mechanism of cervical cancer

  • Authors:
    • Yi Wu
    • Xi Zhou
    • Peng-Sheng Zheng
  • View Affiliations

  • Published online on: June 15, 2011     https://doi.org/10.3892/or.2011.1345
  • Pages: 717-724
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Abstract

CD147, a multifunction glycoprotein of the immuno­globulin family, is associated with many types of tumors, and the overexpression of CD147 can enhance malignancy. However, the role of CD147 in cervical cancer remains unclear. In the present study, cervical cancer cells were found to express much more CD147 protein and isoform‑4 than normal cervical cells (P<0.05), suggesting that CD147 and isoform‑4 are involved in cervical cancers. Furthermore, we overexpressed the CD147 isoform‑4 (CD147‑4) in the cervical cancer cell line SiHa by transfection and found that CD147-4 promoted the proliferation of SiHa cells with a considerable proportion of cells in the S phase in which the expression of CIP2A, Plk and cyclin D1 was up-regulated while the expression of P27 was down-regulated. This may be one of the molecular mechanisms involved in cervical cancer progression by CD147.

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September 2011
Volume 26 Issue 3

Print ISSN: 1021-335X
Online ISSN:1791-2431

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Spandidos Publications style
Wu Y, Zhou X and Zheng P: Involvement of CD147 isoform‑4 in the proliferation of SiHa cells: A possible molecular mechanism of cervical cancer. Oncol Rep 26: 717-724, 2011
APA
Wu, Y., Zhou, X., & Zheng, P. (2011). Involvement of CD147 isoform‑4 in the proliferation of SiHa cells: A possible molecular mechanism of cervical cancer. Oncology Reports, 26, 717-724. https://doi.org/10.3892/or.2011.1345
MLA
Wu, Y., Zhou, X., Zheng, P."Involvement of CD147 isoform‑4 in the proliferation of SiHa cells: A possible molecular mechanism of cervical cancer". Oncology Reports 26.3 (2011): 717-724.
Chicago
Wu, Y., Zhou, X., Zheng, P."Involvement of CD147 isoform‑4 in the proliferation of SiHa cells: A possible molecular mechanism of cervical cancer". Oncology Reports 26, no. 3 (2011): 717-724. https://doi.org/10.3892/or.2011.1345