Research On The Correlation Between MicroRNA-1246and The Pathogenetic Mechanism For Cervical Cancer

Cervical cancer is the serious risk of women’healthy, it is the second common cancer after breast cancer for gynecologic malignancies. Its main reason is that continuous infection of high-risk human papilloma virus (HPV). HPVE6is mainly early control gene associated with the carcinogenicity of HPV. MicroRNAs are a class of small non-coding RNA molecule with17to25nt length, by binging with3’end untranslated regions (3’-UTR) of downstream target genes, and restrain the translation process, to regulating its postranscription progress. In recent years, many studies have shown that microRNAs widely participate in various diseases, including cancer development, and microRNAs can be a molecular marker of disease diagnosis or prognosis also be a potential therapeutic target. MicroRNAs can affect cancer cell proliferation, migration, invasion, cell cycle and apoptosis in cancer development. MicroRNA-1246(miR-1246) is located on chromosome2in human, its expression is regulated by the tumor-suppressor protein p53, participate in the down’s syndrome, systemic lupus erythematosus (SLE) development process. This thesis mainly reserch of the correlation of miR-1246and the pathogenetic mechanism for cervical cancer.Firstly,miR-1246expression levels of68cases of cervical cancer tissue and52cases of control specimen were detected by using the method of real-time quantitative PCR, and the sane time the correlation between miR-1246expression levels and clinicalpathological features was analyzed. The result showed the miR-1246expression levels of cervical cancer group were significantly lower than those of the control group(p<0.05), and the miR-1246expression levels of cervical cancer was associated with clinical stage(p<0.05), but no correlation were found among miR-1246expression levels, age, tumor diameter, cervical invasion depth, lymph node metastasis, and vascular invasion(p>0.05).Based on miR-1246expression levels was found to be significantly lower in the HPV16(+) cervical cancer tissue and cell lines than in no HPV16infection cervical cancer tissue and cell lines. So, the relationship between HPV16E6oncoprotein and miR-1246expression levels were investigated by overexpressing or silencing HPV16E6gene, The miR-1246expression level was increased when knocking out HPV16E6gene in HPV16(+) cervical cancer cell line SiHa, and the downstream target protein DYRKIA was reduced. Similarly, the miR-1246expression level was decreased when transfecting HPV16E6gene in HPV16(-) cervical cancer cell line C33A, with DYRKIA increased. It indicated that HPV16E6oncoprotein was obviously negative regulate the expression of miR-1246.Moreover, the influence of C33A cell proliferation, migration and cell cycle were evaluated through transfecting miR-1246mimics or inhibitor to over express or interfer endogenous miR-1246. We found that miR-1246did not affect the cell proliferation and cell cycle of C33A, but it will affect its cell migration ability.