Effects of Antrodia camphorata on viability, apoptosis, [Ca2+]i, and MAPKs phosphorylation in MG63 human osteosarcoma cells

• Published in: Drug development research 2007-03, Vol.68 (2), p.71-78
• Main Authors: Lu, Yih-Chau, Huang, Chorng-Chih, Huang, Chun-Jen, Chu, Sau-Tung, Chi, Chao-Chuan, Su, Hsing-Hao, Hsu, Shu-Shong, Wang, Jue-Long, Chen, I-Shu, Liu, Shiuh-Inn, Huang, Jong-Khing, Ho, Chin-Man, Kuo, San-Jung, Jan, Chung-Ren
• Format: Article
• Language: English
• Subjects: Antrodia camphorata; apoptosis; Ca2; MAPKs; MG63 cells; osteosarcoma
• ISSN: 0272-4391; 1098-2299
• DOI: 10.1002/ddr.20168

The present study explored the effect of Antrodia camphorata (AC) on viability, apoptosis, mitogen‐activated protein kinases (MAPKs) phosphorylation, and Ca2+ regulation in MG63 human osteosarcoma cells. AC (25–50 µg/ml) did not affect cell viability, but at 100–200 µg/ml decreased viability and induced apoptosis in a concentration‐dependent manner. AC at concentrations of 25–200 µg/ml did not alter basal [Ca2+]i, but at 25 µg/ml decreased [Ca2+]i increases induced by ATP, bradykinin, histamine, and thapsigargin. ATP, bradykinin, and histamine increased cell viability while thapsigargin decreased it. AC (25 µg/ml) pretreatment failed to alter bradykinin‐ and thapsigargin‐induced effects on viability, but potentiated ATP‐ and histamine‐induced increases in viability. Immunoblotting showed that MG63 cells did not have background phospho‐JNK and phospho‐p38 mitogen‐activated protein kinases (MAPKs); and AC did not induce the phosphorylation of these two MAPKs. Conversely, the cells had significant background phospho‐ERK MAPK that was inhibited by 200 µg/ml AC. The ERK‐specific inhibitor PD98059 also induced cell death. Collectively, in MG63 cells, AC exerted multiple effects on viability and [Ca2+]i, caused apoptosis probably via inhibition of ERK MAPK phosphorylation. Drug Dev Res 68:71–78, 2007. © 2007 Wiley‐Liss, Inc.