transcriptional suppression of e-cadherin by hpv-16 e6 and e7 oncogenes is independent of hypermethylation of e-cadherin promoter
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abstract
results hpv-16 e6 and e7 proteins reduced e-cadherin expression 3.7 and 2.2 times when compared with control cells (p = 0.0221 and p = 0.0461, respectively). this reduction was greater in hpv-16 e6-expressing cells than in hpv-16 e7-expressing cells. although hpv-16 e6 and e7 increased dna methyltransferase 1 expression 2.6 and 3.4 times, respectively (p = 0.0133 and p = 0.0113) when compared with control cells, they was no e-cadherin promoter methylation. materials and methods real-time pcr and western blot were used to determine the effects of hpv-16 e6 and e7 on e-cadherin, dnmt1, dnmt3a, and dnmt3b expression in hct-116 cell line. we also analyzed e-cadherin promoter methylation in cells expressing hpv-16 e6 and e7 oncoproteins by bisulfite sequencing. conclusions unlike other cancer-associated viruses (hbv, hcv, and ebv), reduction in e-cadherin expression in hpv-16 e6- and e7-expressing cells is not due to hypermethylation of the e-cadherin promoter. background cervical cancer is one of the most common cancers observed in women worldwide, and its development is related to e6 and e7 two viral oncoproteins of high-risk human papillomavirus (hpv) types. aberrant expression of e-cadherin, which is associated with epithelial-to-mesenchymal transition (emt), is frequently observed in cervical cancer. objectives the mechanisms underlying e-cadherin suppression in cervical cancer are not clear; therefore, this experimental study from iran was designed to elucidate the relationship of dna methyltransferase expression and e-cadherin promoter methylation with e-cadherin expression in hpv-16 e6- and e7-expressing cells.
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Journal title:
iranian red crescent medical journalجلد ۱۹، شماره ۲، صفحات ۰-۰
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