LINC00511 promotes lung squamous cell carcinoma proliferation and migration via inhibiting miR-150-5p and activating TADA1.

Abstract

BackgroundRecently, accumulating data have supported that long non-coding RNAs (lncRNAs) may contribute to tumorigenesis. LncRNA LINC00511 (LINC00511) has been proved to serve as an oncogene in several tumors. However, as a novel lncRNA, the crucial role and potential mechanism of LINC00511 in LUSC is largely unknown.MethodsHere, we performed a differential gene expression analysis of the LINC00511 in LUSC using data from TCGA database. Loss-of-functional assays were used to gain further insights into the latter function of LINC00511 on the malignant phenotypes in vitro. Meanwhile, qRT-PCR, western blot, dual-luciferase reporter, and RIP assays were utilized to highlight the molecular basis of LINC00511 in LUSC.ResultsLINC00511 was upregulated in LUSC tissues in TCGA database compared to adjacent non-tumor counterparts, and its expression level was strongly associated with tumor stage. LINC00511 deficiency significantly suppressed LUSC cell proliferation and migration. Furthermore, mechanistic investigation demonstrated that LINC00511 accelerated LUSC progression partially through its up-regulation of TADA1 via targeting miR-150-5p.Conclusionsour study highlights that LINC00511 facilitates LUSC progression via sequestering miR-150-5p and targeting TADA1, suggesting a need for development of a strategy for therapeutic targeting of LINC00511 in LUSC.