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Article

The role of human papillomavirus type 16 E6/E7 oncoproteins in cervical epithelial-mesenchymal transition and carcinogenesis

  • Authors:
    • Ya-Min Cheng
    • Cheng-Yang Chou
    • Yi-Chiang Hsu
    • Ming-Jenn Chen
    • Lih-Yuh C. Wing
  • View Affiliations / Copyright

    Affiliations: Department of Obstetrics and Gynecology, College of Medicine, National Cheng Kung University Hospital, Tainan 704, Taiwan, R.O.C., Graduate Institute of Medical Science and Innovative Research Center of Medicine, College of Health Sciences, Chang Jung Christian University, Tainan, Taiwan, R.O.C., Division of Traumatology, Department of Surgery, Chi Mei Medical Center, Tainan, Taiwan, R.O.C., Department of Physiology, College of Medicine, National Cheng Kung University Hospital, Tainan 704, Taiwan, R.O.C.
  • Pages: 667-671
    |
    Published online on: December 5, 2011
       https://doi.org/10.3892/ol.2011.512
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Abstract

Cervical cancer is the most common malignancy in females worldwide. This study investigated the prevalence of the E6/E7 oncoproteins of human papillomavirus (HPV) type 16, which are important in fibroblast growth factor (FGF) 2- and 4-induced epithelial-mesenchymal transition (EMT) and cervical tumorigenesis. We investigated the functional interaction between HPV16 E6/E7-transfected Cx cells (CxWJ cells) and treatment with FGF2 and 4, according to the expression of α-smooth muscle actin (α-SMA), vimentin and E-cadherin protein as well as cell growth and invasive ability. The results showed the upregulation of α-SMA and vimentin and the downregulation of E-cadherin protein expression in CxWJ cells. HPV16 E6/E7 infection partially repressed proliferation, but not the invasive ability of FGF2 or FGF4 stimulation in cervical cancer cells (CxWJ cells). These data provide evidence of a functional interaction between HPV16 E6/E7 and FGFs 2 and 4, suggesting that cooperative stimulation of HPV E6/E7 and FGFs activated in human cervical cancer cells is required to completely overcome the oncogenic function associated with the development of cervical epithelial-mesenchymal transition and tumorigenesis.
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Copy and paste a formatted citation
Spandidos Publications style
Cheng Y, Chou C, Hsu Y, Chen M and Wing LC: The role of human papillomavirus type 16 E6/E7 oncoproteins in cervical epithelial-mesenchymal transition and carcinogenesis. Oncol Lett 3: 667-671, 2012.
APA
Cheng, Y., Chou, C., Hsu, Y., Chen, M., & Wing, L.C. (2012). The role of human papillomavirus type 16 E6/E7 oncoproteins in cervical epithelial-mesenchymal transition and carcinogenesis. Oncology Letters, 3, 667-671. https://doi.org/10.3892/ol.2011.512
MLA
Cheng, Y., Chou, C., Hsu, Y., Chen, M., Wing, L. C."The role of human papillomavirus type 16 E6/E7 oncoproteins in cervical epithelial-mesenchymal transition and carcinogenesis". Oncology Letters 3.3 (2012): 667-671.
Chicago
Cheng, Y., Chou, C., Hsu, Y., Chen, M., Wing, L. C."The role of human papillomavirus type 16 E6/E7 oncoproteins in cervical epithelial-mesenchymal transition and carcinogenesis". Oncology Letters 3, no. 3 (2012): 667-671. https://doi.org/10.3892/ol.2011.512
Copy and paste a formatted citation
x
Spandidos Publications style
Cheng Y, Chou C, Hsu Y, Chen M and Wing LC: The role of human papillomavirus type 16 E6/E7 oncoproteins in cervical epithelial-mesenchymal transition and carcinogenesis. Oncol Lett 3: 667-671, 2012.
APA
Cheng, Y., Chou, C., Hsu, Y., Chen, M., & Wing, L.C. (2012). The role of human papillomavirus type 16 E6/E7 oncoproteins in cervical epithelial-mesenchymal transition and carcinogenesis. Oncology Letters, 3, 667-671. https://doi.org/10.3892/ol.2011.512
MLA
Cheng, Y., Chou, C., Hsu, Y., Chen, M., Wing, L. C."The role of human papillomavirus type 16 E6/E7 oncoproteins in cervical epithelial-mesenchymal transition and carcinogenesis". Oncology Letters 3.3 (2012): 667-671.
Chicago
Cheng, Y., Chou, C., Hsu, Y., Chen, M., Wing, L. C."The role of human papillomavirus type 16 E6/E7 oncoproteins in cervical epithelial-mesenchymal transition and carcinogenesis". Oncology Letters 3, no. 3 (2012): 667-671. https://doi.org/10.3892/ol.2011.512
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