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作 者:张燕 张红蕊 孟丹丹 弋振营 李宁 徐志巧 ZHANG Yan;ZHANG Hongrui;MENG Dandan;YI Zhenying;LI Ning;XU Zhiqiao(Kaifeng Central Hospital Tumor Diagnosis and Treatment Center,Kaifeng,Henan 475000,China)
机构地区:[1]开封市中心医院肿瘤诊疗中心,河南开封475000
出 处:《临床肺科杂志》2024年第3期392-399,共8页Journal of Clinical Pulmonary Medicine
摘 要:目的探讨LncRNA CDC6(CDC6)对肺癌细胞增殖、上皮间质转化(epithelial-mesenchymal transition,EMT)和凋亡的影响及其作用机制。方法RT-qPCR检测肺癌组织和细胞中CDC6和c-Myc的mRNA水平,并分析CDC6和c-Myc mRNA水平与患者临床指标的相关性。随后,通过CDC6-siRNA和pcDNA-CDC6转染,或CDC6-siRNA和pcDNA-c-Myc共转染肺癌细胞;MTT法检测细胞增殖能力;流式细胞术检测细胞凋亡;Western Blotting检测增殖、凋亡及EMT相关蛋白的表达。结果LncRNA CDC6在肺癌组织和细胞系中高表达(P<0.05)。CDC6和c-Myc mRNA水平与肺癌的病理分型、TNM分期、分化程度以及淋巴结的转移密切相关。沉默CDC6抑制肺癌细胞增殖,促进细胞凋亡,降低增殖相关蛋白以及EMT相关蛋白表达水平,促进促凋亡蛋白Bax表达,抑制抗凋亡蛋白Bcl-2表达(P<0.05)。过表达CDC6促进肺癌细胞增殖,抑制细胞凋亡,上调增殖相关蛋白以及EMT相关蛋白表达,减少促凋亡蛋白Bax水平,增加抗凋亡蛋白Bcl-2水平(P<0.05)。过表达c-Myc逆转了沉默CDC6对A549细胞增殖、凋亡以及EMT相关蛋白表达的影响。结论LncRNA CDC6通过调控c-Myc促进EMT过程及肺癌细胞的增殖能力,抑制细胞凋亡。Objective To explore the effect and mechanism of lncRNA CDC6 on lung cancer cell proliferation,epithelial-mesenchymal transition(EMT),and apoptosis.Methods The mRNA levels of CDC6 and c-Myc in lung cancer tissues and cells were detected by RT-qPCR,and the correlation between CDC6 and c-Myc mRNA levels and clinical indicators of patients was analyzed.Subsequently,lung cancer cells were transfected with CDC6-siRNA and pcDNA-CDC6,or CDC6-siRNA and pcDNA-c-Myc co-transfected.Cell proliferation was detected by MTT assay.Flow cytometry was used to detect apoptosis.The expressions of proliferation,apoptosis,and EMT-related proteins were detected by Western Blotting.Results Silting CDC6 inhibited the proliferation of lung cancer cells,promoted apoptosis,decreased the expression levels of proliferation-related proteins and EMT-related proteins,promoted the expression of pro-apoptotic protein Bax,and inhibited the expression of anti-apoptotic protein Bcl-2(P<0.05).Overexpression of CDC6 promoted the proliferation of lung cancer cells,inhibited cell apoptosis,up-regulated the expression of proliferation-related proteins and EMT-related proteins,decreased the level of pro-apoptotic protein Bax,and increased the level of anti-apoptotic protein Bcl-2(P<0.05).Overexpression of c-Myc reversed the effects of CDC6 silencing on proliferation,apoptosis,and EMT-related protein expression in A549 cells(P<0.05).Conclusion LncRNA CDC6 promoted the EMT process and the proliferation of lung cancer cells by regulating c-Myc,and inhibited cell apoptosis.
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