Objective To explore the effect of inhibiting the expression of miR-762 on the proliferation and apoptosis of papillary thyroid cancer (PTC) cells TPC-1 and its mechanism. Methods, The qRT-PCR method was used to detect the expression of miR-762 and Bcl-2-like protein 13 (BCL2L13) mRNA in 83 cases of PTC cancer tissues and adjacent tissues, and the correlation between the expression levels of them was analyzed. Bioinformatics prediction software and dual luciferase reporter gene experiment were used to analyze the targeting relationship between miR-762 and BCL2L13. The liposome method was used to transfect miR-762 inhibitor and BCL2L13 siRNA interference plasmid (si-BCL2L13) into TPC-1 cells. qRT-PCR was used to measure the relative transcript levels of miR-762 and BCL2L13, cell proliferation level was detected by MTT and BrdU staining, apoptosis level was detected by flow cytometry, the expression levels of BCL2L13, Cleaved-caspase-3 and cytochrome C (Cyt C) in mitochondria and cytoplasm were detected by Western blot. Results Compared with the adjacent tissues, the expression level of miR-762 increased in PTC cancer tissues, while the expression level of BCL2L13 mRNA decreased, and there was a negative correlation between the two (r=-0.70, P<0.01). The double luciferase reporter gene experiment confirmed that BCL2L13 was the target gene of miR-762. Inhibition of miR-762 expression could significantly down-regulate the expression level of miR-762 in TPC-1 cells, up-regulate the expression of BCL2L13 mRNA and protein, inhibit cell proliferation, increase the level of apoptosis, and up-regulate the expression level of Cleaved-caspase-3 protein and cytoplasmic Cyt C protein, decrease the expression level of mitochondrial Cyt C protein. Interference with BCL2L13 gene expression could notably down-regulate BCL2L13 mRNA and protein expression in TPC-1 cells, promote cell proliferation, inhibit cell apoptosis, up-regulate mitochondrial Cyt C protein expression, and decrease Cleaved-caspase-3 protein and Cyt C protein expression in cytoplasm. In addition, interference with BCL2L13 gene expression could significantly reverse the inhibitory effect of miR-762 inhibitor on TPC-1 cell proliferation and the promotion of miR-762 inhibitor on apoptosis. Conclusion miR-762 is highly expressed in human PTC tissues, and inhibition of miR-762 expression can induce TPC-1 cell apoptosis and inhibit cell proliferation. The mechanism may be related to the targeted up-regulation of BCL2L13 gene expression