Objective This study aimed to explore the role and potential mechanism of miR-30 in EMT of gallbladder cancer ( GBC). Methods qRT-PCR was used to measure the relative expression level of miR-30 in gallbladder epithelial cells and cancer cell lines. After overexpression of miR-30, MTT and colony formation assays were used to assess cell proliferation. Wound healing and Transwell assays were used to evaluate cell migratory and invasive abilities, respectively. Western blot was used to evaluate the expression levels of EMT-related proteins (E-cadherin, Ncadherin and Vimentin) and EMT-related transcription factors (Snail, Slug and Zeb2). A rescue experiment was carried to explore the regulatory relationship between miR-30 and Zeb2. Results miR-30 was significantly downregulated in two representative GBC cell lines ( GBC-SD and NOZ) ( P< 0.05). Overexpression of miR-30 inhibited GBC-SD cell proliferation, colony formation, migration, invasion and EMT ( P< 0.05). Overexpression of Zeb2 reverses the EMT inhibitory effect caused by miR-30 (P<0.05). Conclusions miR-30 attenuates EMT of GBC cells by targeting Zeb2,which indicates that miR-30 is a tumor suppressor and can be used as a novel therapeutic target for GBC.