本文選題：結(jié)直腸癌 + KISS基因��； 參考：《重慶醫(yī)科大學(xué)學(xué)報》2017年11期

【摘要】：目的:探討PKC信號通路在KISS1基因發(fā)揮抑制結(jié)直腸癌細胞HCT116侵襲遷移的作用。方法:構(gòu)建p GC-LV-KISS1-EGFP慢病毒載體感染人結(jié)直腸癌細胞HCT116,分空白對照組(CON組)、空載體對照組(NC組)、過表達組(OE組)。q RT-PCR和Western blot檢測KISS1基因m RNA和Metastin、PKC信號通路的關(guān)鍵分子PKCα、PKCβII及下游E鈣黏蛋白表達量的變化。Transwell法檢測細胞侵襲、遷移能力的變化。結(jié)果:轉(zhuǎn)染后能夠穩(wěn)定表達報告基因EGFP,熒光率均80%,且OE組KISS1基因m RNA、Metastin表達量較CON組和NC組均明顯升高(P0.05)。轉(zhuǎn)染后,PKCβⅡ的蛋白表達量(0.288 2±0.023 7)較CON組(0.530 9±0.013 3)和NC組(0.511 7±0.008 5)明顯下降(P0.05),而PKCα的表達水平無明顯變化(P0.05);下游效益蛋白E鈣黏蛋白表達量(0.633 2±0.017 4)較CON組(0.232 2±0.019 6)和NC組(0.252 3±0.018 2)明顯升高(P0.05)。OE組細胞侵襲、遷移能力較CON組和NC組均明顯下降(P0.05)。結(jié)論:KISS1基因可能通過下調(diào)PKCβⅡ后上調(diào)下游蛋白E鈣黏蛋白的表達而發(fā)揮抑制結(jié)直腸癌細胞HCT116侵襲、遷移作用,有望成為防治結(jié)直腸癌轉(zhuǎn)移的新靶點。
[Abstract]:Aim: to investigate the role of PKC signaling pathway in inhibiting invasion and migration of colorectal cancer cell line HCT116. Methods: HCT116 cells infected with pGC-LV-KISS1-EGFP lentivirus vector were divided into blank control group (Con group), empty vector control group (NC group), overexpression group (OE group). Q RT-PCR and Western blot were used to detect KISS1 gene mRNA and PKC 偽 PKC 尾 II signal pathway. The expression of E-cadherin was detected by Transwell method. A change in mobility. Results: EGFP could be expressed stably after transfection, the fluorescence rate was 80%, and the expression of KISS1 gene m RNA-Metastin in OE group was significantly higher than that in Con group and NC group (P0.05). After transfection, the protein expression of PKC 尾 鈪，

本文編號：2054047