CircSATB2调节miR-150-5p/PDCD4轴对非小细胞肺癌细胞恶性生物学行为的影响  

Impact of circSATB2 on malignant biological behaviors of non-small cell lung cancer cells by regulating miR-150-5p/PDCD4 axis

作　　者：毛维 郭玲 MAO Wei;GUO Ling(Department of Oncology,Xianyang Central Hospital,Shaanxi,Xianyang 712000,China;不详)

机构地区：[1]陕西省咸阳市中心医院肿瘤内科,712000 [2]陕西省咸阳市第一人民医院病理科

出　　处：《河北医药》2025年第2期181-187,共7页Hebei Medical Journal

基　　金：陕西省重点研发计划项目(编号:2017SF-368)。

摘　　要：目的探讨环状RNA(CircRNA)SATB2调节miR-150-5p/程序性细胞死亡因子4(PDCD4)轴对非小细胞肺癌(NSCLC)细胞恶性生物学行为的影响。方法实时荧光定量PCR(qRT-PCR)、免疫组织化学分别检测NSCLC组织、癌旁组织中CircSATB2、miR-150-5p、PDCD4蛋白表达;qRT-PCR、Western blot分别检测人正常肺上皮细胞系BEAS-2B及NSCLC细胞系HCC827、H1299、A549中CircSATB2、miR-150-5p、PDCD4蛋白表达;将A549细胞分为对照组(NC组)、抑制对照组、CircSATB2抑制组、上调对照组、miR-150-5p上调组、CircSATB2抑制+inhibitor NC组、CircSATB2抑制+miR-150-5p inhibitor组,qRT-PCR检测各组细胞CircSATB2、miR-150-5p表达;CCK-8法检测细胞增殖;流式细胞术检测细胞凋亡;划痕实验检测细胞迁移;Transwell检测细胞侵袭;Western blot检测PDCD4、增殖细胞核抗原(PCNA)、BCL-2相关X蛋白(Bax)、基质金属蛋白酶(MMP)-2、MMP-9蛋白表达;CircSATB2与miR-150-5p/PDCD4关系验证。结果确定以A549细胞为研究细胞模型;与抑制对照组比较,CircSATB2抑制组CircSATB2、PDCD4蛋白降低,miR-150-5p表达升高(P<0.05);与上调对照组比较,miR-150-5p上调组PDCD4蛋白降低,miR-150-5p表达升高(P<0.05);与CircSATB2抑制+inhibitor NC组比较,CircSATB2抑制+miR-150-5p inhibitor组miR-150-5p表达降低,PDCD4蛋白升高(P<0.05);抑制CircSATB2或上调miR-150-5p均可减弱A549细胞增殖、侵袭、迁移能力,增强细胞凋亡行为;下调miR-150-5p减弱了抑制CircSATB2对A549细胞增殖、侵袭、迁移及凋亡的影响;CircSATB2靶向调控miR-150-5p/PDCD4。结论抑制CircSATB2可能通过调控miR-150-5p/PDCD4减弱A549细胞增殖、迁移与侵袭能力,增强凋亡行为。Objective To investigate the impact of circular RNA(circRNA)SATB2 on the malignant biological behaviors of non-small cell lung cancer(NSCLC)cells by regulating the miR-150-5p/programmed cell death 4(PDCD4)axis.Methods The expressions of CircSATB2,miR-150-5p and PDCD4 proteins in NSCLC tissues and paracancerous tissues were detected by quantitative real time polymerase chain reaction(qRT-PCR)and immunohistochemistry.Their expressions in human normal pulmonary epithelial cell line BEAS-2B and NSCLC cell lines HCC827,H1299 and A549 were detected by qRT-PCR and Western blot.A549 cells were treated with blank control,or transfected with circSATB2 overexpression plasmid,circSATB2 knockdown plasmid,circSATB2 negative control(NC)plasmid,miR-150-5p NC,miR-150-5p mimic,circSATB2 knockdown plasmid+inhibitor NC,and circSATB2 knockdown plasmid+miR-150-5p inhibitor.The expression of CircSATB2 and miR-150-5p was detected by qRT-PCR.Cell proliferation was detected by cell counting kit-8(CCK-8)assay.Apoptosis was detected by flow cytometry.Cell migration was detected by wound healing assay.Cell invasion was detected by Transwell assay.Western blot was used to detect the protein expressions of PDCD4,proliferating cell nuclear antigen(PCNA),Bcl-2 associated X protein(Bax),matrix metalloproteinase(MMP-2)and MMP-9.The relationship between CircSATB2 and miR-150-5p/PDCD4 was verified.Results A549 cells were selected as the in vitro model.Knockdown of circSATB2 significantly downregulated circSATB2 and PDCD4,but upregulated miR-150-5p(P<0.05).Overexpression of miR-150-5p significantly downregulated PDCD4 and upregulated miR-150-5p(P<0.05).Co-k nockdown of circSATB2 and miR-150-5p significantly downregulated miR-150-5p and upregulated PDCD4 than A549 cells with knockdown of circSATB2(P<0.05).Knockdown of circSATB2 or overexpression of miR-150-5p inhibited proliferation,invasion and migration of A549 cells,but stimulated cell apoptosis.Knockdown of miR-150-5p weakened the regulatory effect of circSATB2 on the proliferation,invasion,migrat

关 键 词：环状RNA SATB2 miR-150-5p 程序性细胞死亡因子4 非小细胞肺癌 增殖 

分 类 号：R734.2[医药卫生—肿瘤]