Abstract:

Long Jia, Li Liming, Xu Cui, Yang Jia, Jiang Mingjun Department of Dermatology, Shenzhen Second People's Hospital, The First Affiliated Hospital of Shenzhen University，Shenzhen 518035, China （Long J）; Institute of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College; Jiangsu Key Laboratory of Molecular Biology for Skin Diseases and STIs, Nanjing 210042, China （Li LM, Xu C, Yang J, Jiang MJ) Corresponding author: Jiang Mingjun, Email: drmingjunjiang@163.com 【Abstract】 Objective To evaluate effects of human papilloma virus （HPV） 16E7 on s of six tumor suppressor genes （including MT1G, NMES1, RRAD, SFRP1, SPARC and TFPI2） in a cell line SiHa, as well as on its proliferation and apoptosis. Methods SiHa cells were divided into two groups to be transfected with a small interfering RNA targeting HPV16E7 （E7SiRNA, experimental group） and an empty vehicle （negative control group） respectively, with SiHa cells receiving no treatment serving as the blank control group. After 48 hours, qPCR was performed to measure the mRNA s of E7 and six tumor suppressor genes, CCK-8 assay to evaluate cellular proliferative activity, and flow cytometry to assess apoptosis of SiHa cells. Results At 48 hours after the transfection, the experimental group showed significantly decreased E7 mRNA （0.25 ± 0.036, P < 0.05）, but increased mRNA s of the six genes （MT1G 1.403 ± 0.190, NMES1 1.720 ± 0.060, RRAD 1.390 ± 0.160, SFRP1 1.493 ± 0.120, SPARC 2.157 ± 0.144, TFPI2 2.060 ± 0.122, all P < 0.05）. The proliferative activity of SiHa cells was significantly decreased （0.554 ± 0.130 vs. 1.028 ± 0.236 and 1.220 ± 0.126, both P < 0.05）, but the apoptosis rate was significantly increased （9.222% vs. 0.246% and 0.123%, both P < 0.05） in the experimental group compared with the negative control group and blank control group. No significant differences were observed between the negative control group and blank control group in proliferative activity or apoptosis rate of SiHa cells （both P > 0.05）. Conclusion E7 may participate in HPV16-induced cellular malignant transformation by suppressing the mRNA s of 6 tumor suppressor genes, including MT1G, NMES1, RRAD, SFRP1, SPAR and TFPI2.