【摘要】 目的 探究缺氧微环境处理肾癌细胞来源的外泌体通过ERK5信号通路影响细胞的增殖和凋亡的相关机制。方法 以ACHN细胞为研究对象，构建缺氧微环境。按处理方式分为缺氧组和正常组，收集上述2组细胞的外泌体，检测标志物CD63分子和CD81分子的表达，检测细胞的增殖，检测ERK5和凋亡相关基因的mRNA表达水平，检测ERK5和凋亡相关基因的蛋白表达水平，检测细胞的凋亡。结果 外泌体为直径50～150 nm的双层膜囊泡状结构。外泌体的分子标志物CD81和CD63表达阳性。缺氧组的外泌体可以通过缩短有丝分裂的时间，促进肿瘤细胞的增殖。缺氧组的癌细胞的增殖能力明显高于正常组（P<0.01）,ERK5、Caspase-3和Bad的表达水平明显低于正常组（P<0.01），而抗凋亡因子Bcl-2的表达则明显高于正常组（P<0.05）。结论 缺氧环境下，肾癌细胞来源的外泌体可以通过ERK5信号通路促进细胞的增殖，抑制凋亡。更多还原

【Abstract】 Objective To explore the mechanism by which exosomes derived from renal cancer cells treated with hypoxic microenvironment affect cell proliferation and apoptosis through the ERK5 signaling pathway. Methods A hypoxic microenvironment was constructed with ACHN cells as the research object. The cells were divided into hypoxia group and normal group according to the treatment method. The exosomes of the cells were collected. The expressions of CD63 and CD81, cell proliferation, the mRNA expression of ERK5 and apoptosis-related genes were detected. Results The exosomes were doublelayer membrane vesicle-like structures with a diameter of 50-150 nm. The CD81 and CD63 of exosomes were positive. In the hypoxia group, exosomes promoted the proliferation of cells by shortening the time of mitosis, the proliferation of cancer cells was significantly higher than that in the normal group(P<0. 01), the expressions of ERK5, Caspase-3 and Bad were significantly lower(P<0. 01), and the expression of Bcl-2 was significantly higher(P<0. 05). Conclusion In hypoxic environment, exosomes derived from renal cancer cells can promote cell proliferation and inhibit apoptosis through the ERK5 signaling pathway.更多还原