摘要
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 bio-function of EPO and EPOR in the cancer progression of NSCLC. Methods： 27 NSCLC tissues were recruited. The expression levels of EPO and EPOR were analyzed in 27 NSCLC tissues by immunohistochemistry（IHC）. The cell viability and cell cycle were detected in HCC15 and HCC1819 cells under recombinant human EPO（rh EPO）. EPO and EPOR expression were observed in HCC15 and HCC1819 under hypoxia. Results： EPO and EPO-R expression were up-regulated in NSCLC samples. The expression rate of EPO expression was observed in 48 %（13 of 27） NSCLC. The expression rate of EPOR was up-regulated in 92 %（25 of 27） NSCLC. In vitro, rh EPO obviously increased the numbers of colony formation of EPOR up-regulating HCC1819 cells, whereas rh EPO had no effect on the numbers of colony formation of EPOR down-regulating HCC15 cells. Meanwhile,rh EPO enhanced the viability of HCC1819 cells. Knockdown of EPOR via si RNA decreased the viability induced by rh EPO. rh EPO significantly promoted HCC1819 cell cycle. Hypoxia up-regulated EPO expression and then increased cell viability in HCC1819 cells.Conclusion： EPO and EPOR are up-regulated in NSCLC. EPO promotes cancer progression of NSCLC via EPOR. Hypoxia increases the levels of EPO in NSCLC.
出处
《现代生物医学进展》
CAS
2015年第28期5428-5431,5454,共5页
Progress in Modern Biomedicine
基金
国家自然科学基金项目(81100001)
