LINC02163在肺腺癌中过表达并促进肺腺癌增殖和侵袭

LINC02163 is Overexpressed in Lung Adenocarcinoma and Promotes Proliferation and Invasion of Lung Adenocarcinoma Cells

目的观察长链非编码RNA LINC02163对肺腺癌(lung adenocarcinoma,LUAD)侵袭和增殖能力的影响,并探讨其机制.方法实时荧光聚合酶链反应(RT-PCR)检测人支气管上皮细胞株(BEAS-2B)和LUAD细胞(A549和Calu-3)中LINC02163的表达水平;生物信息学分析获取LINC02163相关结合蛋白;在LUAD中抑制LINC02163表达后,Western印迹检测TAF15的表达水平;在LUAD细胞中抑制LINC02163后,再过表达TAF15,应用EdU,CCK-8与Transwell实验评估细胞增殖和侵袭能力的改变.结果与BEAS-2B比较,LUAD细胞中LINC02163的表达水平均明显升高(P<0.05);TAF15是LINC02163潜在的结合蛋白;抑制LINC02163表达后LUAD细胞中TAF15表达下调;LUAD细胞敲降LINC02163后,细胞增殖和侵袭能力明显减弱(P<0.05),而过表达TAF15后增殖和侵袭能力明显恢复(P<0.05);LINC02163对LUAD恶性表型的影响是通过TAF15实现的.结论LINC02163可通过上调TAF15的表达促进LUAD细胞的增殖和侵袭.

Objective To examine the effect of long non-coding RNA LINC02163 on the invasion and proliferation of lung adenocarcinoma(LUAD),and to explore its mechanism.Methods The expression of LINC02163 in normal bronchial epithelial cells(BEAS-2B)and LUAD cells(A549 and Calu-3)was detected by real-time fluorescent quantitative PCR(RT-PCR).Bioinformatics analysis was performed to obtain the LINC02163 associated binding protein.The expression of TAF15 in LUAD cells after knockdown of LINC02163 was examined by Western blotting.The proliferation and invasion of LUAD cells after LINC02163 knockdown and TAF15 overexpression were examined by EdU,CCK-8 and Transwell assay.Results The expression levels of LINC02163 in LUAD cells were significantly increased as compared with those in BEAS-2B cells(P<0.05).TAF15 was a potential binding protein of LINC02163.Transfection with siRNA LINC02163 down-regulated TAF15 expression(P<0.05).In LUAD cells,the abilities of cell proliferation and invasion were significantly reduced after UNC02163 knockdown(P<0.05),which could be reversed by the overexpression of TAF15(P<0.05).The effect of LINC02163 on LUAD malignant phenotype was achieved through TAF15.Conclusion LINC02163 can promote the proliferation and invasion of LUAD cells by up-regulating the expression of TAF15.