本文選題：p　切入點：喉癌　出處：《中國病理生理雜志》2017年06期

【摘要】：目的:探討p62在喉癌細胞Hep-2化療耐藥中的作用及潛在的作用機制。方法:實時熒光定量聚合酶鏈式反應(RT-q PCR)及Western blot法檢測喉癌耐藥細胞Hep-2/5-FU及其親本細胞Hep-2中p62的表達水平。在Hep-2/5-FU細胞中轉(zhuǎn)染p62 siRNA敲減p62的表達,采用CCK-8法和流式細胞術(shù)檢測細胞生存率及細胞凋亡狀態(tài);檢測細胞中丙二醛(malondialdehyde,MDA)的含量及超氧化物歧化酶(superoxide dismutase,SOD)、谷胱甘肽過氧化物酶(glutathione peroxidase,GSH-Px)的活性來反映細胞氧化應激水平。Western blot檢測細胞凋亡相關(guān)調(diào)控因子Bcl-2、Bax、caspase-8/cleaved caspase-8、caspase-3/cleaved caspase-3的蛋白水平及抗氧化通路Keap1/Nrf2的活性。結(jié)果:耐藥細胞株Hep-2/5-FU中p62的mRNA及蛋白表達水平均明顯高于親本細胞株Hep-2;并且在親本細胞株Hep-2中,p62和Nrf2的蛋白表達水平隨著順鉑的濃度增加不斷升高。沉默p62可抑制喉癌耐藥細胞Hep-2/5-FU的生存,促進其凋亡,上調(diào)MDA的含量,降低SOD和GSH-Px的活性,同時上調(diào)Bax、cleaved caspase-8、cleaved caspase-3和Keap1的蛋白水平,下調(diào)Bcl-2、Nrf2及HO-1的蛋白表達。結(jié)論:喉癌耐藥細胞Hep-2/5-FU中沉默p62可恢復細胞對5-FU的敏感性,其機制可能與抑制Keap1/Nrf2信號通路的活化、調(diào)控細胞內(nèi)氧化應激反應及細胞凋亡有關(guān)。
[Abstract]:Objective: to investigate the role and potential mechanism of p62 in Hep-2 chemotherapeutic resistance of laryngeal carcinoma cells.Methods: Real-time quantitative polymerase chain reaction (RT-q PCR) and Western blot were used to detect the expression of p62 in Hep-2/5-FU and its parent cells.The expression of p62 siRNA knockout p62 was transfected into Hep-2/5-FU cells. The survival rate and apoptosis were detected by CCK-8 and flow cytometry.媯，

本文編號：1702161