LINC00116 enhances cervical cancer tumorigenesis through miR-106a/c-Jun pathway.

Abstract

Some studies imply that LINC00116 is involved in cervical cancer progression; however, the molecular mechanism by which LINC00116 modulating tumorigenesis of cervical cancer remains not clear. Reverse transcription-quantitative PCR (RT-qPCR)and the Western blot approaches were employed to probe genes expression levels. To examine the tumorigenic abilities of cervical cancer cells, MTT assay, Transwell assay, and wound-healing assay were used to investigate proliferation, invasion, and migration of HeLa or C-33A cells. LINC00116 knockdown attenuates cell proliferation, invasion, and migration of cervical cancer cells. miR-106a directly binds LINC00116 and regulate each other. Moreover, miR-106a inhibitor remarkably enhanced tumorigenesis of shLINC00116 HeLa cells. Through bioinformatic and dual-luciferase reporter assay, the results showed that miR-106a mimic directly targeted and downregulated the c-Jun. c-Jun overexpression could greatly rescue miR-106a mimic-modulated cervical cancer tumorigenesis. LINC00116 knockdown and miR-106a mimic-modulated programmed cell death ligand 1 (PD-L1) expression, which could be reverted by c-Jun introduction. LINC00116, PD-L1, and JUN were both upregulated in cervical cancer tumors compared to normal tissues. Lower expression levels of LINC00116 and JUN, as well as higher level of miR-106a were closely associated with higher overall survival of cervical cancer patients. Here, we report a novel role for LINC00116 in tumorigenesis of cervical cancer by regulating miR-106a/c-Jun axis. Our findings provide a foundation for understanding cervical cancer and facilitate the development of therapeutical approaches by targeting LINC00116.