| Abstract |
Cervical cancer is the second cause of death among female cancer and strongly implicated with high-risk human papillomavirus (HR-HPV) infection, especially HPV16. However, HPV infection alone is not sufficient for cancer development. Thus, other cofactors are necessary to HPV-induced carcinogenesis of cervix. We investigated the effect of estradiol, the most potent naturally occurring estrogen, on proliferation of cervical cancer cell lines, oncogene expression and HPV16 LCR variant transcriptional activity. Cervical cell lines were treated with various concentration of estradiol and cell viability was determined. SiHa cell line was treated with estradiol to evaluate E6 gene expression using real time PCR. For transcriptional assay, C33A cells were transfected with vector containing the LCR of HPV16 European (E) prototype or Asian (As) variant and then treated with 40 nM and 100 nM estradiol for 48 h. The result found that estradiol did not affect on cell proliferation but induced E6 expression up to 1.5 fold and the transcriptional activity of LCR. Only 100 nM estradiol treatment, HPV16 E prototype LCR showed significant higher than untreated (P <0.000). In contrast, HPV16 As variant LCR, estradiol significantly increased transcriptional activity in a dose dependent manner (P = 0.028). Moreover, LCR transcriptional activity of HPV16 As variant was induced more than HPV16 E prototype. These evidences showed an important association of estradiol as a co-factor of HR-HPV infection, especially HPV16 As variant, which mostly found in Asian patients including Thai woman. |
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Journal Publication
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