LINC01619 promotes non-small cell lung cancer development via regulating PAX6 by suppressing microRNA-129-5p.

This article explored LINC01619 impact on non-small cell lung cancer (NSCLS) development. LINC01619 expression in tumor tissues/normal tissues of NSCLS patients was detected by qRT-PCR and in situ hybridization. PAX6 expression in clinical tissues was researched by immunohistochemistry. After transfection, SPCA1 and A549 cells were subjected to CCK-8 assay and cell colony formation experiment. Xenograft tumor experiment was conducted. ALDH+ cells from SPCA1 and A549 cells were separated and transfected. ALDH+ cells percentage, sphere number and cancer stem cell markers expression was determined by flow cytometry, sphere culture and Western blot respectively. Luciferase reporter gene assay and RNA binding protein immunoprecipitation assay was conducted. The colocalization of LINC01619 and miR-129-5p in cells was determined by RNA fluorescence in situ hybridization experiment. Gene expression in tissues and cells were assessed by qRT-PCR and Western blot. As a result, aberrantly up-regulated LINC01619 and PAX6 in NSCLC patients predicted poor prognosis. LINC01619 overexpression in SPCA1 cells enhanced cell viability, cloning ability, and xenograft tumors volume and weigh, whereas LINC01619 silencing in A549 cells weakened the above indicators. LINC01619 overexpression promoted cancer stem cells characteristics including increasing percentage of ALDH+ cells, sphere number and cancer stem cell markers expression. LINC01619 directly inhibited miR-129-5p and the two genes were mainly colocalized in the cytoplasm. PAX6 was up-regulated in NSCLC and directly suppressed by miR-129-5p. LINC01619 promoted cells viability, cloning ability and cancer stem cells characteristics in NSCLC via the miR-129-5p/PAX6 axis. Thus, LINC01619 promotes NSCLC development via regulating PAX6 by suppressing miR-129-5p.