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目的研究缺氧诱导因子-1α(HIF-1α)和程序性死亡因子配体1(PD-L1)在肺腺癌中的表达与临床病理特征的关系,探讨肺腺癌中HIF-1α对PD-L1的调控作用。方法应用免疫组织化学方法检测99例肺腺癌组织中HIF-1α、PD-L1的表达。Co Cl2模拟化学性缺氧处理肺腺癌细胞,并将其分为正常组及CoCl_2组,qRT-PCR检测HIF-1α、PD-L1 mRNA表达,Western blotting检测HIF-1α、PD-L1蛋白表达。siRNA-HIF-1α瞬时转染肺腺癌细胞,并将其分为阴性对照组及siR-HIF-1α组,qRT-PCR、Western blotting检测转染效率及PD-L1 mRNA和蛋白的表达。结果 99例肺腺癌组织中,HIF-1α和PD-L1的阳性率分别为47.48%和34.34%,HIF-1α表达水平与患者年龄和临床分期有关(P<0.05),PD-L1表达水平与患者临床分期有关(P<0.05),HIF-1α蛋白表达与PD-L1蛋白表达呈正相关(P<0.01)。与正常组相比,CoCl_2组细胞中HIF-1α蛋白表达水平明显升高(t=-2.394,P=0.029),PD-L1 mRNA及蛋白表达水平随之明显升高(t=-3.146,P=0.006;t=-3.308,P=0.004)。与阴性对照组相比,siR-HIF-1α组沉默处理细胞后,PD-L1 mRNA及蛋白表达水平显著降低(t=2.746,P=0.014;t=2.339,P=0.033)。结论肺腺癌组织中HIF-1α和PD-L1明显共表达;PD-L1表达受HIF-1α调控。
Objective To investigate the relationship between the expression of hypoxia-inducible factor-1α (HIF-1α) and apoptosis-associated ligand 1 (PD-L1) in lung adenocarcinoma and the clinicopathological features of HIF-1α in lung adenocarcinoma -L1 regulatory role. Methods The expression of HIF-1α and PD-L1 in 99 cases of lung adenocarcinoma was detected by immunohistochemistry. Co Cl2 was used to simulate hypoxia-treated lung adenocarcinoma cells. The cells were divided into normal group and CoCl 2 group. The mRNA expression of HIF-1α and PD-L1 was detected by qRT-PCR. The protein expressions of HIF-1α and PD-L1 were detected by Western blotting . siRNA-HIF-1α was transiently transfected into lung adenocarcinoma cells and divided into negative control group and siR-HIF-1α group. The transfection efficiency and the expression of PD-L1 mRNA and protein were detected by qRT-PCR and Western blotting. Results The positive rates of HIF-1α and PD-L1 in 47 cases of lung adenocarcinoma were 47.48% and 34.34%, respectively. The expression of HIF-1α was related to the age and clinical stage (P <0.05) (P <0.05). There was a positive correlation between HIF-1α protein expression and PD-L1 protein expression (P <0.01). Compared with the normal group, the expression of HIF-1α in CoCl_2 group was significantly increased (t = -2.394, P = 0.029), the expression of PD-L1 mRNA and protein was significantly increased (t = -3.146, P = 0.006; t = -3.308, P = 0.004). Compared with the negative control group, the expression of PD-L1 mRNA and protein in siR-HIF-1α group was significantly decreased (t = 2.746, P = 0.014; t = 2.339, P = 0.033). Conclusions The expression of HIF-1α and PD-L1 in lung adenocarcinoma is obviously co-expressed. The expression of PD-L1 is regulated by HIF-1α.