Taken together, our findings provide the first clues regarding the role of miR-193a-3p as a tumor suppressor in lung cancer through the inhibition of ERBB4 translation.

MiR-193a-3p inhibited the metastasis of lung cancer cells by deregulating the expression of tumor-related proteins.

Conclude that UCA1 functions as an oncogene in non-small cell lung carcinoma, acting mechanistically by upregulating ERBB4 in part through 'spongeing' miR-193a-3p.

Results show that MiR-193a expression is decreased due to DNA hypermethylation in non-small cell lung cancers specimens. Restoration of miR-193a inhibits migration, invasion, and TGF-beta1-induced EMT through modulating WT1-E-cadherin axis.

miR-193a displayed its role in lung cancer via modulating the HMGB1 expression. This study demonstrated that UCA1 exerts oncogenes activity in lung cancer, acting mechanistically by upregulating HMGB1 expression through 'sponging' miR-193a.

High miR193 expression is associated with metastasis of lung cancer.

STAT3-induced LINC00668 contributed to non-small cell lung cancer progression through upregulating KLF7 expression by sponging miR-193a.