Journal
ONCOTARGET
Volume 6, Issue 27, Pages 23930-23943Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.4525
Keywords
HPV16 E6 and E7; DNA methylation; immunoblot; cell viability and apoptosis; human cervical carcinoma cell lines
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Funding
- National Natural Science Foundation of China [31470274]
- Jiangsu Key Laboratory of Molecular Biology for Skin Diseases and STIs [2012ZD006]
- Jiangsu Provincical Special Program of Medical Science [BL2012003]
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In SiHa and CaSki cells, E6 and E7-targeting shRNA specifically and effectively knocked down human papillomavirus (HPV) 16 E6 and E7 at the transcriptional level, reduced the E6 and E7 mRNA levels by more than 80% compared with control cells that expressed a scrambled-sequence shRNA. E6 and E7 repression resulted in down-regulation of DNA methyltransferase mRNA and protein expression, decreased DNA methylation and increased mRNA expression levels of tumor suppressor genes, induced a certain apoptosis and inhibited proliferation in E6 and E7 shRNA-infected SiHa and CaSki cells compared with the uninfected cells. Repression of E6 and E7 oncogenes resulted in restoration of DNA methyltransferase suppressor pathways and induced apoptosis in HPV16-positive cervical carcinoma cell lines. Our findings suggest that the potential carcinogenic mechanism of HPV16 through influencing DNA methylation pathway to activate the development of cervical cancer exist, and maybe act as a candidate therapeutic strategy for cervical and other HPV-associated cancers.
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