LINC01197调控Notch通路促进肺腺癌细胞增殖和侵袭

LINC01197 regulates Notch pathway to promote lung adenocarcinoma cell proliferation and invasion

目的揭示LINC01197在肺腺癌中的表达情况及其潜在机制。方法实时荧光定量PCR(qRT-PCR)检测LINC01197表达,免疫印迹检测Notch信号分子(Notch1和Hes1)表达。MTT、集落形成和Transwell实验分析细胞增殖和侵袭能力。异种移植瘤实验检测LINC01197对肿瘤生长的影响。结果肺腺癌中LINC01197下调,Notch1和Hes1的蛋白水平均上调(P<0.05)。LINC01197过表达抑制肺腺癌细胞增殖和侵袭,而敲低LINC01197具有相反的效果(P<0.05)。LINC01197诱导的细胞行为变化可以被Notch1调节剂逆转(P<0.05)。LINC01197过表达抑制体内肿瘤生长和Notch信号传导(P<0.05)。结论LINC01197可能通过抑制Notch信号通路在肺腺癌中表现出抗增殖、抗侵袭作用。

Objective To reveal the expression and underlying mechanism of LINC01197 in lung adenocarcinoma(LUAD).Methods The expression of LINC01197 was detected by real-time fluorescence quantitative PCR(qRT-PCR),and the expression of Notch signaling molecules(Notch1 and Hes1)were detected by Western blot.Cell proliferation and invasion ability were analyzed by MTT,colony formation and Transwell assays.The effect of LINC01197 on tumor growth was examined in a xenograft tumor assay.Results LINC01197 was down-regulated in LUAD,and the protein levels of Notch1 and Hes1 were both up-regulated(P<0.05).Overexpression of LINC01197 inhibited LUAD cell proliferation and invasion,while knockdown of LINC01197 had the opposite effect(P<0.05).Interestingly,LINC01197-induced changes in cell behavior could be reversed by Notch1 modulators(P<0.05).Furthermore,LINC01197 overexpression inhibited tumor growth and Notch signaling in vivo(P<0.05).Conclusion LINC01197 can exhibit anti-proliferation and anti-invasion effects in LUAD by inhibiting Notch signaling pathway.