Macroautophagy (also known as autophagy) is a main route for sequestration and digestion of cytoplasm in acidic compartments in order for cancer cells to survive from nutrient depletion, chemotherapy or other insults.In the present study, we characterized the role of miR-30d in the crosstalk between autophagy and apoptosis, which determines the sensitivity of anaplastic thyroid cancer (ATC) cells to cisplatin.We found that treatment with cisplatin caused activation of autophagy in ATC cell lines, SW1736 and 8305C.We further demonstrated that forced expression of miR-30d significantly reduced cisplatin-induced autophagy, resulting in increased cisplatininduced cytotoxicity.Moreover, inhibition of autophagy and sensitization to cisplatin by forced expression of miR-30d were accompanied by induction of apoptosis.To confirm that the sensitizing effect of miR-30d on the cytotoxicity of cisplatin was attributed to suppression of autophagy, we assessed the effects of the autophagy inhibitors 3-MA and chloroquine.Treatment with 3-MA and chloroquine strongly increased cisplatin-induced apoptosis, indicating that blockade of autophagy indeed renders ATC cells sensitivity to cisplatin.Finally, an in vivo ATC implantation mouse model clearly showed that elevation of miR-30d significantly enhanced cisplatininduced apotosis in implanted tumor cells.By using molecular and biochemistry assays, we found that the autophagy-related gene Beclinl, can be directly regulated by miR-30d in cancer cells.Our results not only revealed a new mechanism determining cisplatin sensitivity, but also identified miR-30d as a novel autophagy regulator which can target Beclinl.Thus, that increasing miR-30d level maybe exploited a novel approach to enhance the efficacy ofcisplatin against ATC or other types of malignancies.