Long non-coding RNA UCA1 promotes lung cancer cell proliferation and migration via microRNA-193a/HMGB1 axis

Highlights: • UCA1 affected the cellular function in lung cancer cells. • microRNA-193a played important role by regulating HMGB1 expression in lung cancer cells. • UCA1 exerted its role via modulation of UCA1/microRNA-193a/HMGB1 axis in lung cancer cells. Lung cancer is a leading cause of death worldwide. Long non-coding RNAs have been documented aberrantly expressed and exerted crucial role in variety of cancers. Urothelial carcinoma associated 1 (UCA1) is a potential new type of biomarkers for tumor diagnosis and exerts oncogenic effect on various human cancers. However, the mechanism of oncogenic role of UCA1 in lung cancer remains unclear. In this study, we firstly confirmed the role of UCA1 in lung cancer and found that UCA1 down-regulation inhibited cell proliferation and migration in both SKMES-1 and H520 lung cancer cells. Then we demonstrated that repressed UCA1 promoted the miR-193a expression and miR-193a could bind to the predicted binding site of UCA1. We then dissected the role of miR-193a in lung cancer and proved the anti-tumor role of miR-193a. Furthermore, we found that miR-193a displayed its role in lung cancer via modulating the HMGB1 expression. In addition, we found that over-expression of HMGB1 could restore the UCA1 knockdown induced repression of cell proliferation and migration. In summary, our study demonstrated that UCA1 exerts oncogenes activity in lung cancer, acting mechanistically by upregulating HMGB1 expression through 'sponging' miR-193a.