Long non-coding RNA HOTAIR functions as a competitive endogenous RNA to regulate PRAF2 expression by sponging miR-326 in cutaneous squamous cell carcinoma

Abstract

Abstract Background LncRNAs may exert a regulatory effect in tumorigenesis. Although the expression of lncRNA HOTAIR has been confirmed to be notably elevated in the tissues of CSCC, its biological mechanism in CSCC is still unknown. Methods HOTAIR expression level in CSCC cell lines was monitored via qRT-PCR. Then CCK-8 assay, Transwell assay and EdU assay were adopted to detect cell migration and proliferation. Meanwhile, through bioinformatics analysis and luciferase reporter gene detection, a new target of HOTAIR was identified. Additionally, Western blotting and RIP analysis were adopted to discuss the possible mechanism. Results HOTAIR expression in CSCC cell lines exhibited an obvious elevation. Cell function analysis revealed that HOTAIR overexpression remarkably facilitated CSCC cell migration, proliferation and EMT process, which were impeded by down-regulation of HOTAIR. Furthermore, HOTAIR competitively bound to miR-326, so as to positively modulate miR-326 expression. Conclusions These results present that HOTAIR, as a ceRNA, regulates PRAF2 expression by competitive binding to miR-326 during CSCC.