Despite surgery and adjuvant therapy, early-stage lung adenocarcinoma (LUAD) treatment often fails due to local or metastatic recurrence. However, the mechanism is largely unknown.Here, we report that increased expression levels of miR-134-5pand decreased levels of disabled-2 (DAB2) were significantlycorrelated with recurrence in stage I LUAD patients. Ourdata show that miR-134-5p overexpression or DAB2 silencingstrongly stimulated LUAD cell metastasis and chemoresistance.In contrast, inhibition of miR-134-5p or overexpression ofDAB2 strongly suppressed LUAD cell metastasis and overcamethe insensitivity of chemoresistant LUAD cells to chemotherapy. In addition, we demonstrated that DAB2 is a targetof miR-134-5p and that miR-134-5p stimulates chemoresistance and metastasis through DAB2 in LUAD. Taken together,these findings suggest that miR-134-5p and its target geneDAB2 have potential as a biomarker for predicting recurrencein stage I LUAD patients. Additionally, miR-134-5p inhibitionor DAB2 restoration may be a novel strategy for inhibitingLUAD metastasis and overcoming LUAD cell resistance tochemotherapy.