Human Papillomavirus (HPV) 16
infection is considered as one of the significant causes of human
cervical cancer. The expression of the viral oncogenes like E6 and E7 play an important role in the development of the
cancer. MiR-122 has been reported to exhibit a strong relationship with hepatitis viruses and take part in several
tumor development, while the effects of miR-122 on
HPV infection and the HPV viral oncogenes expression still remain unexplored. In this study, using RNAhybrid software, the potential binding sites between miR-122 and HPV16 E6 and E7 mRNAs were identified. Over and loss of miR-122 function showed that miR-122 could directly bind with HPV16 E6
mRNA and significantly inhibit its expression in SiHa cells, which was further confirmed by constructing the miR-122-E6-mu to eliminate the miR-122 binding effects with E6. The increase of the expression of
type I interferon (IFN) and its classical effective molecules and the phosphorylation of signal transducers and activators of transcription (
STAT1) protein indicated that miR-122 might enhance
type I interferon in cervical
carcinoma cells, which explained the significant reduction of HPV16 E7 and E6*I
mRNA expression. This might be due to the binding between miR-122 and suppressor of
cytokine signaling 1 (SOCS1)
mRNA, which is the suppressor of
interferon signaling pathway. Moreover, it was identified that the miR-122 binding position was nt359-nt375 in SOCS1
mRNA. Taken together, this study indicated that HPV16 could be effectively inhibited by miR-122 through both direct binding with E6
mRNA and promoting SOCS1-dependent IFN signaling pathway. Thus, miR-122 may serve as a new therapeutic option for inhibiting
HPV infection.