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Purpose has been confirmed, high-risk human papillomavirus (HR HPV) infection is a major cause of cervical cancer, but it is not the only cause of disease. Studies have shown that folic acid deficiency have increased the risk of cervical cancer. Folic acid as a carbon donor units involved in DNA methylation. The study found that abnormal DNA methylation in tumorigenesis are closely related. CpG island hypermethylation of the promoter region of the tumor suppressor gene p16 is an important reason that causes cervical cancer. Play a major role in the process of DNA methylation DNA methyltransferase (DNMT), a variety of tumor cells were found in of DNMT the abnormally high expression. The above events to be linked in cervical lesions, and what interactions currently very little research in this area. The subject as HPV16-positive and HPV-negative cervical cancer cells in the the different folate concentrations intervention, the proliferation of the cells was observed, detection of p16, DNMT1 protein and mRNA expression in both cell lines, and the analysis of the above events in cervical cancer relationship. Square method to select the HPV16 positive cervical cells Caski in and HPV-negative cervical cancer cells C33A routinely cultured to logarithmic phase cells take various cell lines of different folate concentrations intervention MTT assay was used to observe the effects of folic acid on the two cell activity; through cells count, the cell growth curve to explore the effects of folic acid on two cervical cancer cell proliferation; using real-time quantitative PCR (real timePCR) detection HPV16 oncogene E2, E6, expression of p16, and DNMT1mRNA; Western blotting, two cell p16 and DNMT1 protein expression. Use the SPSS16.0 software analysis data, normal distribution using t test, analysis of variance, Pearson correlation and linear regression, the level of information Spearman correlation. 1, folic acid activity of two cervical cancer cells was inhibited and different folic acid concentrations In addition to the C33A cells 50ug/ml and 100ug/ml outside, other experimental group compared to the control group, the difference was statistically significant (P lt; 0.05), and in the same folic acid concentrations, folic acid a statistically significant difference between the inhibition of the activity of Caski and C33A cells (P lt; 0.05), and stronger than inhibition of Caski cells C33A cells inhibited. Cell count found that when folic acid concentration 50ug/ml and above, compared to their control group, the experimental group, the total number of cells in both cell lines significantly reduced, and the difference was statistically significant (P lt; 0.05); With folate concentrations increased, the inhibitory effect of folic acid on cell enhancement. 2, p16 expression in cervical cancer cells: different folic acid concentrations, C33A and Caski cells, p16mRNA expression of the protein expression differences were statistically the significance (p16mRNA expression: C33A cells F = 2.969, P = 0.034; Caski cell F = 3.186, P = 0.026; protein expression: C33A cells F = 68.821, P lt; 0.001; Caski cells F = 36.674, P lt; 0.001), and with folate concentrations increased the C33A lineage p16mRNA expression lower (P lt; 0.001) higher (P = 0.006), protein expression in p16mRNA Caski cells (P = 0.496), decreased expression of p16 protein expression decreased (P lt; 0.001); same folic acid concentrations the, Caski cells p16mRNA C33A expression and protein than cell lines (P lt; 0.05); under the different expressions of DNMT1 expression in cervical cancer cell folate concentrations, Caski cell folate concentrations group difference DNMT1mRNA expression, protein expression differences were significant (DNMT1mRNA expression: F = 30.633, P lt; 0.001; protein expression: F = 32.214, P lt; 0.001), and increased with folate concentrations, DNMT1mRNA expression and protein expression were decreased to reduce (P lt; 0.05) DNMT1 protein expression; C33A cells the difference was statistically significant (F = 73.67, P lt; 0.001), with folic acid concentration increased expressions of DNMT1 protein expression were lower (P lt; 0.05); same folic acid concentrations C33A cell lines (P lt; 0.05), DNMT1mRNA expression and protein expression is higher than in the Caski cells; 4, Caski cells HPV16 oncogene E2, E6 expression folate concentrations the E2, E6mRNA expression of the difference was not statistically significant ( E2: F = 3.246, P = 0.111; E6: F = 2.641, P = 0.150). Summary 1, folic acid can inhibit the growth of cervical cancer cells Caski and C33A, and folic acid concentration increased inhibition enhanced; the same folate concentrations, compared C33A strong inhibition of folic acid on Caski cell proliferation, suggesting folic acid and HPV16 infection cervical cancer cells. 2, folic acid can affect the tumor suppressor gene the p16mRNA and protein expression in cervical cancer cells, p16 protein can reduce folate supplementation, mRNA expression was elevated; HPV16 infection can increase the chance of high expression of the p16. 3, folic acid, and cervical cancer cells DNMT1mRNA and protein expression, folic acid supplementation can make DNMT1mRNA and protein expression decreased; HPV16 infection influential DNMT1 expression. 4, folic acid impact on the HPV16 oncogenes Caski cells transcriptional level may be weak.
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