LncRNA LOXL1-AS1 promotes invasion and proliferation of non-small-cell lung cancer through targeting miR-324-3p.

LncRNAs are played crucial roles in athogenesis of NSCLC. LOXL1-AS1 involved in development of several tumors. So far, there is no study about expression and function pattern of the LOXL1-AS1 in NSCLC. In this reference, we firstly proved that LOXL1-AS1 was overexpressed in NSCLC cell lines (H23, A549, H1299 and SPC-A1) compared to 16HBE cell. The expression of LOXL1-AS1 was overexpressed in NSCLC specimens than adjacent control specimens. We found that 29 of 40 cases showed higher LOXL1-AS1 expression in NSCLC samples as compared to adjacent control specimens. Ectopic expression of LOXL1-AS1 promoted H1299 cell and H23 cell proliferation. LOXL1-AS1 overexpression promoted ki-67 and cyclin D1 expression in the NSCLC cell. Overexpression of LOXL1-AS1 promoted cell invasion and induced N-cadherin and Vimentin expression and suppressed E-cadherin expression in the NSCLC cell. LOXL1-AS1 acts as one sponge for miR-324-3p in NSCLC cell. Moreover, the expression of miR-324-3p was lower in NSCLC specimens than adjacent control specimens. We found that 24 of 40 cases showed lower miR-324-3p expression in NSCLC samples as compared to adjacent control specimens. Further correlation assay indicated a negative association between miR-324-3p and LOXL1-AS1 expression. miR-324-3p restoration attenuates the function of LOXL1-AS1 overexpression on NSCLC cell. These results indicated that LOXL1-AS1 enhanced NSCLC cell proliferation and invasion via sponging miR-324-3p in NSCLC cell. AJTR