CAJ | 학술논문

目的观察肿瘤坏死因子相关诱导凋亡配体(TRAIL)联合蛋白酶抑制剂MG132对人肺腺癌细胞GLC-82增殖的抑制和血小板衍生生长因子受体α(PDGFRα)-磷脂酶Cγ1(PLCγ1)-蛋白激酶Cα(PKCα)信号转导通路的影响.方法用噻唑蓝(MTT)法检测TRAIL联合蛋白酶抑制剂MG132对GLC-82细胞生长的抑制作用;采用流式细胞仪技术检测TRAIL联合蛋白酶抑制剂MG132对GLC-82细胞凋亡的影响,采用链霉菌抗生物素蛋白-过氧化物酶(SP)免疫组织化学法检测TRAIL联合蛋白酶抑制剂MG132相关蛋白PDGFRα、PLCγ1、PKCα的表达,Western blot测定TRAIL联合蛋白酶抑制剂MG132对GLC-82细胞PDGFRα、PLCγ1、PKCα蛋白表达的影响.结果 MTI法显示TRAIL联合蛋白酶抑制剂MG132作用GLC-82细胞株后,抑制率较单独应用TRAIL和MG132均显著增高,抑制率分别为(34.92±3.95)％、(33.17±1.78)％和(76.96±1.28)％(P＜0.05);流式细胞仪细胞凋亡检测结果显示,TRAIL联合蛋白酶抑制剂MG132作用GLC-82细胞48 h后TRAIL联合蛋白酶抑制剂MG132能明显诱导GLC-82细胞凋亡(P＜0.05),免疫组织化学检测结果显示TRAIL联合蛋白酶抑制剂MG132作用GLC-82细胞株后能使PDGFRα、PLCγ1、PKCα蛋白表达降低,Western blot结果显示TRAIL联合蛋白酶抑制剂MG132明显抑制PDGFRα、PLCγ1、PKCα蛋白的表达.结论 TRAIL联合蛋白酶抑制剂MG132对人肺腺癌GLC-82细胞的生长有明显的抑制作用,能降低GLC-82细胞PDGFRα-PLCγ1-PKCα信号通路各蛋白表达的水平,肺腺癌的发病和PDGFRα-PLCγ1-PKCα转导通路信号增强关系密切.
목적 관찰종류배사인자상관유도조망배체(TRAIL)연합단백매억제제MG132대인폐선암세포GLC-82증식적억제화혈소판연생생장인자수체α(PDGFRα)-린지매Cγ1(PLCγ1)-단백격매Cα(PKCα)신호전도통로적영향.방법 용새서람(MTT)법검측TRAIL연합단백매억제제MG132대GLC-82세포생장적억제작용;채용류식세포의기술검측TRAIL연합단백매억제제MG132대GLC-82세포조망적영향,채용련매균항생물소단백-과양화물매(SP)면역조직화학법검측TRAIL연합단백매억제제MG132상관단백PDGFRα、PLCγ1、PKCα적표체,Western blot측정TRAIL연합단백매억제제MG132대GLC-82세포PDGFRα、PLCγ1、PKCα단백표체적영향.결과 MTI법현시TRAIL연합단백매억제제MG132작용GLC-82세포주후,억제솔교단독응용TRAIL화MG132균현저증고,억제솔분별위(34.92±3.95)％、(33.17±1.78)％화(76.96±1.28)％(P＜0.05);류식세포의세포조망검측결과현시,TRAIL연합단백매억제제MG132작용GLC-82세포48 h후TRAIL연합단백매억제제MG132능명현유도GLC-82세포조망(P＜0.05),면역조직화학검측결과현시TRAIL연합단백매억제제MG132작용GLC-82세포주후능사PDGFRα、PLCγ1、PKCα단백표체강저,Western blot결과현시TRAIL연합단백매억제제MG132명현억제PDGFRα、PLCγ1、PKCα단백적표체.결론 TRAIL연합단백매억제제MG132대인폐선암GLC-82세포적생장유명현적억제작용,능강저GLC-82세포PDGFRα-PLCγ1-PKCα신호통로각단백표체적수평,폐선암적발병화PDGFRα-PLCγ1-PKCα전도통로신호증강관계밀절.
Objective To tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) combined with a protease inhibitor MG132 observed in human lung adenocarcinoma cell line GLC-82 inhibition of proliferation and platelet derived growth factor receptor α (PDGFRα)-phospholipase Cγ1 (PLCγ1)-protein kinase Cα (PKCα) signal transduction pathway.Methods Methyl thiazol tetrazolium (MTT) assay inhibition of TRAIL combined with a protease inhibitor MG132 on GLC-82 cell growth detection; using flow cytometry to detect the effects of TRAIL combined with a protease inhibitor MG132 on GLC-82 cell apoptosis,using SP immunohistochemical detection of protease inhibitors MG132 joint expression of TRAIL-associated protein PDGFRα,PLCγ1,PKCα' s,Western blotting to determine the effect of protease inhibitors MG132 TRAIL combined for GLC-82 cells PDGFRα,PLCγ1,PKCα protein expression.Results MTT assay inhibition of TRAIL combined with a protease inhibitor MG132 on GLC-82 cell growth detection.The inhibitory rates were (34.92 ± 3.95) ％,(33.17 ± 1.78) ％ and (76.96 ± 1.28) ％,respectively; using flow cytometry to detect the effects of TRAIL combined with a protease inhibitor MG132 on GLC-82 cell apoptosis.Apoptosis rates of the four group were 6.78％,38.72％,45.60％ and 91.74％,respectively.Using SP immunohistochemical detection of protease inhibitors MG132 joint expression of TRAIL-associated protein PDGFRα,PLCγ1,PKCα's,Western blotting to determine the effect of protease inhibitors MG132 TRAIL combined for GLC-82 cells PDGFRα,PLCγ1,PKCα protein expression.Conclusion TRAIL combined protease inhibitor MG132 on human lung adenocarcinoma GLC-82 cells significantly inhibited the growth,can reduce the level of GLC-82 cells PDGFRα-PLCγ1 -PKCα each protein signaling pathway,the incidence of lung cancer and PDGFRα-PLCγ1-PKCα enhanced signal transduction pathways are closely related.