论文部分内容阅读
Objective: Study on the mechanism of HPV16 E6 gene mutation promoting the proliferation of cervical cancer cells by influencing the expression of BDNF/TrkB. Methods: The expression levels of HPV16 E6 T350G, BDNF, TrkB and p53 mRNA in cervical cancer tissue samples and CINII cervical tissues were detected by Real-time PCR. HPV16 E6 T350G lentivirus(pLV5-HPV16 E6 T350G)and empty vector(pLV5- vector) were designed and constructed, and transfected with HCerEpiC cells, the expression levels of HPV16 E6 T350G, BDNF, TrKB and p53 mRNA were detected by Real-time PCR, and the expression levels of BDNF, TrKB, PI3K, pPI3K, AKT and pAKT protein were detected by western blot;cell proliferation was detected by MTT experiments. Results: Compared with cinii cervical tissue, HPV16 E6 T350G, BDNF and TrkB mRNA expression levels were all positive, while p53 mRNA expression was negative. After overexpression of HPV16 E6 T350G in HCerEpiC cells, it can up-regulate the expression levels of BDNF and TrKB protein and mRNA, and activate the PI3K/AKT signaling pathway which is the downstream of BDNF/TrKB, and reduce p53 protein expression levels; HPV16 E6 T350G overexpression can enhance the proliferation capacity of HCerEpiC cells. Conclusion: Overexpression of HPV16 E6 T350G can promote the proliferation of cervical cancer cells, which may be related to the upregulation of BDNF/TrKB expression, the activation of PI3K/AKT signaling pathway, and the decrease of p53 expression.