Long non-coding RNA GLIDR accelerates the tumorigenesis of lung adenocarcinoma by miR-1270/TCF12 axis.

Lung adenocarcinoma (LUAD) is a deadly cancer with a high incidence worldwide. Long noncoding RNAs (lncRNAs) have been confirmed to have the regulatory effects on the occurrence and development of LUAD. But the specific functions of lncRNA GLIDR in LUAD are still not explicit and need to be investigated. On the basis of the outcomes of RT-qPCR experiments, the relative expression of GLIDR was evidently up-regulated in LUAD cells, while that of miR-1270 was down-regulated. The down-regulation of GLIDR inhibits cell proliferation in accordance with the results of CCK-8, EdU and colony formation assays, and accelerates cell apoptosis according to the results of flow cytometry and JC-1 analyses. Luciferase reporter, RNA pull down and RIP assays indicated that GLIDR could sponge miR-1270 in LUAD. Additionally, TCF12 was proved as the target gene of miR-1270. Furthermore, rescue experiments indicated that overexpression of TCF12 could offset the inhibitory functions of silencing GLIDR on cell behaviors. In brief, this study has demonstrated that GLIDR/miR-1270/TCF12 axis plays the crucial role in LUAD, which offers a new insight into researches on molecular mechanism concerning LUAD and provides with a new perspective for LUAD treatment.