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Abstract
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.