A novel benzofuran derivative, ACDB, induces apoptosis of human chondrosarcoma cells through mitochondrial dysfunction and endoplasmic reticulum stress

摘要: // Chen-Ming Su 1, 2 , Chien-Yu Chen 3 Tingting Lu 1 Yi Sun Weimin Li 4 Yuan-Li Huang 5 Chun-Hao Tsai 6, 7 Chih-Shiang Chang Chih-Hsin Tang 2, 5, 8 Department of Biomedical Sciences Laboratory, Affiliated Dongyang Hospital Wenzhou Medical University, Dongyang, Zhejiang, China Graduate Institute Basic Science, Taichung Taiwan Pharmaceutical Chemistry, Taichung, Cardiology, Biotechnology, College Health Asia 6 School Medicine, Orthopedic Surgery, University Hospital, Pharmacology, Correspondence to: Chang, email: chihshiang3@gmail.com Chih-Hsin, Tang, chtang@mail.cmu.edu.tw Keywords: benzofuran, chondrosarcoma, apoptosis, endoplasmic reticulum (ER) stress, mitochondrial dysfunction Received: August 25, 2016      Accepted: October 19, Published: November 07, 2016 ABSTRACT Chondrosarcoma is one the bone tumor with high mortality in respond to poor radiation and chemotherapy treatment. Here, we analyze antitumor activity a novel benzofuran derivative, 2-amino-3-(2-chlorophenyl)-6-(4-dimethylaminophenyl)benzofuran-4-yl acetate (ACDB), human chondrosarcoma cells. ACDB increased cell apoptosis chondrosarcomas without harm chondrocytes. also enhanced which was characterized by varieties cytosolic calcium levels induced expression glucose-regulated protein (GRP) calpain. Furthermore, ACDB-induced associated upregulation B lymphoma-2 (Bcl-2) family members including pro- anti-apoptotic proteins, downregulation dysfunctional mitochondria that released cytochrome C, subsequent activation caspases-3. In addition, ACDB-mediated cellular suppressed transfecting cells calpain siRNA or treating ER stress chelators caspase inhibitors. Interestingly, animal experiments illustrated reduction volume following Together, these results suggest may be suppressor this study demonstrates agent, ACDB, vitro vivo .