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作 者:郑建洲[1] 白煜[1] 戚春建[1] ZHENG Jianzhou;BAI Yu;QI Chunjian(Medical Research Center,Changzhou Second People’s Hospital,Nanjing Medical University,Changzhou 213100,China)
机构地区:[1]南京医科大学附属常州市第二人民医院中心实验室,常州213100
出 处:《肿瘤防治研究》2022年第6期563-568,共6页Cancer Research on Prevention and Treatment
基 金:国家自然科学基金(81672799);江苏省重点研发计划项目(BE2019651)。
摘 要:目的探讨lncRNA FENDRR对肺鳞癌细胞H226的增殖、迁移、侵袭和凋亡的影响及分子机制。方法qRT-PCR检测肺正常上皮细胞BEAS、肺腺癌细胞A549、H1299和肺鳞癌细胞H226中FENDRR的表达水平。将H226细胞分为FENDRR-siRNA组和FENDRR-siNC阴性对照组;CCK-8法检测细胞增殖活力,Transwell小室检测细胞迁移和侵袭能力;流式细胞术检测细胞凋亡;Western blot检测细胞MEK、p-MEK、ERK、p-ERK蛋白表达。结果与肺正常上皮细胞相比,肺鳞癌细胞H226中FENDRR水平明显下降。下调肺鳞癌细胞H226中FENDRR的表达后,p-MEK和p-ERK蛋白表达水平显著增多,H226细胞增殖活力、迁移及侵袭能力显著增加,细胞凋亡率明显降低。加入ERK抑制剂U0126能逆转FENDRR表达下调对H226细胞的作用。结论低表达FENDRR后,可以通过ERK/MAPK信号通路,促进H226细胞的增殖、迁移和侵袭,并抑制其凋亡。Objective To investigate the effects of lncRNA FENDRR on the proliferation,migration,invasion and apoptosis of LUSC H226 cells and its molecular mechanism.Methods The expression levels of FENDRR in normal lung epithelial cells BEAS,lung adenocarcinoma A549 and H1299 cells and LUSC H226 cells were detected by qRT-PCR.H226 cells were transfected with FENDRR-siRNA as the experimental group,or with FENDRR-siNC as a negative control group.Cell proliferation was detected by CCK-8 assay.Cell migration and invasion were detected by Transwell assay.Cell apoptosis was detected by flow cytometry.The protein expression levels of MEK,p-MEK,ERK and p-ERK were determined by Western blot.Results FENDRR levels in H226 cells were significantly lower than those in normal lung epithelial cells.Compared with the negative control group,the knockdown of FENDRR could significantly promote the proliferation,migration and invasion of H226 cells,inhibit the cell apoptosis,and increase the protein levels of p-MEK and p-ERK.The addition of ERK inhibitor U0126 rescued the effect of FENDRR knockdown on H226 cells.Conclusion The knockdown of lncRNA FENDRR can promote the proliferation,migration and inhibit the apoptosis of H226 cells through ERK/MAPK pathway.
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