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目的:研究促红细胞生成素(erythropoietin,EPO)及其受体(EPOR)在非小性细胞肺癌中的生物学作用。方法:收集27例非小性细胞肺癌(NSCLC),免疫组织化学方法检测肺癌组织中EPO和EPOR的表达;观察人源重组EPO(rh EPO)对HCC15和HCC1819细胞活力和细胞周期的影响;分析缺氧对NSCLC细胞EPO及EPOR表达的影响。结果:27例非小细胞肺癌的组织标本中13例表达EPO,表达率为48%,25例表达EPOR,表达率为92%。rh EPO明显增加了高表达EPOR的HCC1819细胞克隆数,而对低表达EPOR的HCC15细胞的克隆形成没有影响。rh EPO增强了HCC1819的细胞活力,但以si RNA干涉HCC1819EPOR后,EPO对HCC1819细胞活力增强作用消失。rh EPO明显增加了HCC1819细胞的细胞周期。缺氧促进了HCC1819细胞的EPO的表达,增强了细胞活力。结论:EPO和EPOR在非小性细胞肺癌中表达增高,EPO通过EPOR促进了NSCLC细胞的增殖,缺氧诱导了NSCLC细胞EPO的表达。
Objective: To investigate the biological role of erythropoietin (EPO) and its receptor (EPOR) in non-small cell lung cancer. Methods: Twenty-seven non-small cell lung cancer (NSCLC) were collected. The expression of EPO and EPOR in lung cancer tissues were detected by immunohistochemistry. The effect of rh EPO on the viability and cell cycle of HCC15 and HCC1819 cells was analyzed. Effects of hypoxia on the expression of EPO and EPOR in NSCLC cells. Results: Twenty - seven cases of non - small cell lung cancer showed EPO expression in 13 of them, the expression rate was 48% and the expression of EPOR in 25 cases was 92%. rh EPO significantly increased the number of HCC1819 cells highly expressing EPOR, but had no effect on the clonogenicity of HCC15 cells with low expression of EPOR. rh EPO enhanced the cell viability of HCC1819 cells, but the effect of EPO on HCC1819 cell viability disappeared after siRNA interference with HCC1819EPOR. rh EPO significantly increased the cell cycle of HCC1819 cells. Hypoxia promotes the expression of EPO in HCC1819 cells and enhances cell viability. CONCLUSION: EPO and EPOR are highly expressed in non-small cell lung cancer. EPO promotes the proliferation of NSCLC cells through EPOR. Hypoxia induces the expression of EPO in NSCLC cells.