Tauroursodeoxycholic acid mediates endoplasmic reticulum stress and autophagy in adrenocortical carcinoma cells.

Adrenocortical carcinoma (ACC) is an invasive tumor that occurs in the endocrine system. Increasing evidence has shown that endoplasmic reticulum (ER) stress and autophagy play an important role in tumor formation. Tauroursodeoxycholic acid (TUDCA) is an ER chemical chaperone that can alleviate ER stress. In the present study, TUDCA promoted the proliferation, migration and invasion of ACC SW-13 and NCI-H295R cells. Reverse transcription-quantitative PCR and western blot analysis showed that the expression of glucose-regulated protein 78, a promoter of ER stress, was decreased. The expression levels of protein kinase R (PKR)-like ER kinase and activating transcription factor 6 were correspondingly decreased, and the downstream proteins, C/EBP homologous protein and JNK, were also decreased. The expression levels of the autophagy factor microtubule-associated protein light chain 3-II/I and the anti-apoptotic factor Bcl-2 increased following TUDCA treatment, while the expression of the pro-apoptotic factor Bax decreased. TUDCA alleviated ER stress in ACC SW-13 and NCI-H295R cells and induced autophagy, thereby inhibiting ACC cell apoptosis. ER stress- and autophagy-related signaling pathways are involved in the occurrence of ACC, which may provide potential therapeutic targets for ACC treatment.