Abstract: Objective To explore the effects of emodin on the proliferation, apoptosis, migration and invasion of papillary thyroid carcinoma B-CPAP cells and its possible mechanism. Methods B-CPAP cells were divided into five groups: a control group (where the solvent was DMSO), a 20 μmol/L emodin group, a 40 μmol/L emodin group, a 80 μmol/L emodin group, an inhibitor group (80 μmol/L of emodin and the PI3K inhibitor LY294002). The cell viability and proliferation were determined by CCK8 assay and colony formation, respectively. The apoptotic rates were detected by flow cytometry. The cell migration and invasion were assessed by wound healing assay and Transwell assay. The levels of apoptosis-related proteins Bax, Bcl-2, Cleaved caspase-3 and AKT/GSK3β/β-catenin pathway proteins were measured by Western blot. Results Compared with the control group, emodin remarkably inhibits the proliferation, migration, and invasion of B-CPAP cells and promotes the apoptosis of B-CPAP cells in a dose- and time-dependent manner. After emodin treatment, the levels of the AKT/GSK3β/β-catenin signaling pathway-associated proteins were reduced. Meanwhile, no statistical differences were found between the 80 μmol/L group and the inhibitor group (P>0.05). Conclusions Emodin inhibits tumor-related characteristics in B-CPAP cells by inhibiting the Akt/GSK3β/β-catenin pathway.