摘要
目的:探究外泌体微小RNA(miR)-23a对非小细胞肺癌(NSCLC)血管生成的影响,分析其作用机制。方法:收集NSCLC患者癌组织和癌旁组织,同时以人肺癌细胞系H1299细胞为研究对象。比较癌组织与癌旁组织第10号染色体缺失性磷酸酶和张力蛋白同源物基因(PTEN)、血管内皮生长因子(VEGF)表达。分别采用免疫组化染色、酶联免疫吸附测定(ELISA)、实时定量反转录PCR(qRT-PCR)和Western blot分析miR-23a对H1299细胞PTEN、VEGF、蛋白激酶B(AKT)表达的影响。结果:肺癌组织PTEN表达低于癌旁组织,而VEGF表达高于癌旁组织(均P<0.05)。miR-23a过表达明显抑制H1299细胞PTEN mRNA和蛋白表达,促进AKT、VEGF mRNA以及磷酸化AKT(p-AKT)和VEGF蛋白表达,而抑制miR-23a后结果相反(均P<0.05)。结论:NSCLC细胞来源的外泌体miR-23a能够诱导肿瘤血管生成,促进NSCLC的发展,其机制可能与靶向抑制PTEN有关。
Objective:To explore the effect of exosome miR-23a on angiogenesis in non-small cell lung cancer(NSCLC)and analyze its mechanism.Methods:The tumor tissues and paracancerous tissues of NSCLC patients and the human lung cancer cell line H1299 were collected as the research object.The expressions of PTEN and VEGF in tumor tissues and paracancerous tissues were compared.The effects of miR-23a on the expression of PTEN,VEGF and AKT in H1299 cells were analyzed by immunohistochemical staining,ELISA,qRT-PCR and Western blot,respectively.Results:The expression of PTEN in lung cancer tissues was lower than that in paracancerous tissues,while the expression of VEGF was higher than that in paracancerous tissues(all P<0.05).Overexpression of miR-23a significantly inhibited the expressions of PTEN mRNA and protein,and promoted the expressions of AKT,VEGF mRNA and the expressions of p-AKT and VEGF protein in H1299 cells,but the results were opposite after inhibition of miR-23a(all P<0.05).Conclusion:MiR-23a can induce tumor angiogenesis and promote the development of NSCLC,and its mechanism may be related to the targeted inhibition of PTEN.
作者
崔凯
白峻峰
支亚男
姜琨
王壮壮
公孙鑫
CUI Kai;BAI Junfeng;ZHI Ya’nan;JIANG Kun;WANG Zhuangzhuang;GONGSUN Xin(Department of Thoracic Surgery,Xi’an International Medical Center Hospital,Xi’an 710100,China)
出处
《陕西医学杂志》
CAS
2021年第9期1048-1051,1055,共5页
Shaanxi Medical Journal
