Abstract

This study investigates the influence of fibroblast growth factor receptor type B (FGFRb) and fibroblast growth factor on cervical carcinogenesis associated with HPV16 E6/7 infection, using primary cancer cells isolated from Taiwanese patients with cervical cancer. Functional interaction between FGFRb in Cx cells and HPV16 E6/7 transfected Cx cells (CxWJ cells) following treatment with FGF-7, according to cell growth, invasive ability, and tumor growth in SCID mice. Our results indicate that the downregulation of FGFRb gene expression in CxWJ cells partially represses proliferation and the invasive ability provided by FGF-7 stimulation. In SCID mice, the FGF2 and FGFR1 gene expression ascend in CxWJ tumor nodule. These data provide evidence of a functional interaction between HPV16 E6/7 in FGFRb and FGF2, suggesting that cooperative stimulation of HPV E6/7 in inactivated FGFRb and the upregulation of FGF2 may be necessary to completely overcome the oncogenic function associated with the progression of cervical carcinogenesis.

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