MBNL1-AS1 was significantly reduced in NSCLC. Meanwhile, overexpression of MBNL1-AS1 obviously repressed proliferation, blocked cell cycle, promoted apoptosis and inhibited the migration and invasion of NSCLC. Dual-luciferase reporter assay and RIP experiment showed MBNL1-AS1 was able to regulate miR-135a-5p expression negatively to inhibited NSCLC progression.

Lung cancer remains a big threat to human health. Growing evidence has reported the crucial regulatory effect of lncRNAs on NSCLC progression. Nevertheless, the detailed function of lncRNA MBNL1-AS1 involved in NSCLC development is poorly known. In our research, we confirmed that MBNL1-AS1 was significantly reduced in NSCLC patient tissues and NSCLC cells. Meanwhile, we reported that overexpression of MBNL1-AS1 obviously repressed A549 and H1975 cell proliferation, blocked cell cycle and inhibited the migration and invasion. Moreover, A549 and H1975 cell apoptosis was increased by the overexpression of MBNL1-AS1. Then, we predicted that miR-135a-5p was a potential target of MBNL1-AS1 and its level was correlated with MBNL1-AS1 in NSCLC negatively. Our previous study indicated miR-135a-5p could induce lung cancer progression through regulating LOXL4. Here, we found that MBNL1-AS1 was able to regulate miR-135a-5p expression negatively. The direct binding association between MBNL1-AS1 and miR-135a-5p was proved using dual-luciferase reporter assay and RIP experiment. Subcutaneous xenotransplanted tumor model was set up and it was confirmed increased MBNL1-AS1 remarkably restrained tumorigenic ability of NSCLC through sponging miR-135a-5p in vivo. To sum up, our data revealed the significance of the MBNL1-AS1 and miR-135a-5p in NSCLC. In conclusion, MBNL1-AS1 could be a new therapeutic target to treat NSCLC.