Song Z C, Ding L, Ren Z Y, Sun X S, Yang Q, Wang L, Feng M J, Liu C L, Wang J T
Department of Epidemiology, School of Public Health, Shanxi Medical University, Taiyuan 030001, China.
Community Health Centre, Shanxi Cardiovascular Hospital, Taiyuan 030001, China.
Zhonghua Liu Xing Bing Xue Za Zhi. 2017 Sep 10;38(9):1246-1251. doi: 10.3760/cma.j.issn.0254-6450.2017.09.021.
To explore the effect of Src on cervical cancer cells through ERK signal transduction pathway. Experimental study was carried out in vitro. Cervical cancer cell lines Hela (HPV-positive) and C33A (HPV-negative) were treated with Src kinase inhibitor PP2. Then, the cell cycle and apoptosis of each group were evaluated by using flow cytometry (FCM). Western blotting and Real-time PCR were used to detect the levels of the expression of ERK 1/2, c-Fos and c-Jun mRNA and protein respectively. The database was established and analyzed with SPSS statistical software (version 20.0). After down-regulating Src, the cell proliferation was inhibited and cell apoptosis was induced. The proportions of G0/G1 stage of Hela and C33A cell in cell cycle increased while G2/M and S stages decreased. Meanwhile, the mRNA levels of ERK 1, ERK 2, c-Fos and c-Jun increased. And the expression levels of ERK 1/2, phosphorylated ERK 1/2 (p-ERK 1/2) and phosphorylated c-Fos (p-c-Fos) protein decreased, while c-Jun and phosphorylated c-Jun (p-c-Jun) protein expression increased. In addtion, the change level of Hela cell, p-ERK 1/2 and c-Fos protein were lower than that of C33A cell before and after the Src inhibition. Src, involved in regulating the expression of key factors of the ERK signal transduction pathway including p-ERK 1/2 and p-c-Fos, might be capable of promoting the proliferation of cervical cancer cells and inhibiting their apoptosis. The infection with HPV might have adjustable effect on this process.
通过ERK信号转导通路探讨Src对宫颈癌细胞的影响。进行体外实验研究。用Src激酶抑制剂PP2处理宫颈癌细胞系Hela（HPV阳性）和C33A（HPV阴性）。然后，采用流式细胞术（FCM）评估各组细胞周期和凋亡情况。分别用蛋白质免疫印迹法和实时荧光定量PCR检测ERK 1/2、c-Fos和c-Jun mRNA及蛋白的表达水平。使用SPSS统计软件（版本20.0）建立数据库并进行分析。下调Src后，细胞增殖受到抑制，细胞凋亡被诱导。细胞周期中Hela和C33A细胞G0/G1期比例增加，而G2/M期和S期比例降低。同时，ERK 1、ERK 2、c-Fos和c-Jun的mRNA水平升高。ERK 1/2、磷酸化ERK 1/2（p-ERK 1/2）和磷酸化c-Fos（p-c-Fos）蛋白的表达水平降低，而c-Jun和磷酸化c-Jun（p-c-Jun）蛋白表达增加。此外，Src抑制前后，Hela细胞p-ERK 1/2和c-Fos蛋白的变化水平低于C33A细胞。Src参与调节包括p-ERK 1/2和p-c-Fos在内的ERK信号转导通路关键因子的表达，可能促进宫颈癌细胞增殖并抑制其凋亡。HPV感染可能对此过程有调节作用。
