RESUMEN
The aim of the present study was to investigate the effects of shikonin (SHI) on the induction of apoptosis in human TT medullary thyroid carcinoma cells, and to explore the role of mitochondrial signaling in this process. MTT, Annexin Vphycoerythrin/7aminoactinomycin D staining, electron microscopy and JC1 probe staining were performed to analyze mitochondrial membrane potential, and western blot analysis was used to examine the activation of the mitochondrial signaling pathway, and the changes in mitochondrial apoptosis pathwayassociated protein expression. Following culture for 2472 h, treatment with various concentrations of SHI inhibited the proliferation of TT cells, in a dose and timedependent manner. Transmission electron microscopy demonstrated the presence of typical apoptotic structures, as well as mitochondrial structural changes. The expression levels of apoptosisassociated proteins caspase9, caspase3 and poly adenosine triphosphate ribose polymerase increased in a dosedependent manner following treatment with SHI. In addition, the mitochondrial membrane potential of the experimental group was significantly decreased, and the mitochondrial apoptosis pathwayassociated proteins were altered. A possible mechanism underlying SHIinduced apoptosis through the mitochondrial signaling pathway is the regulation of B cell lymphoma 2 (Bcl2)/Bcl2associated protein X expression levels, resulting in the decrease in mitochondrial membrane potential and the activation of the caspase9/caspase3 enzymeassociated reactions.