RT Journal Article SR Electronic T1 Aloe-emodin Induces Cell Death through S-Phase Arrest and Caspase-dependent Pathways in Human Tongue Squamous Cancer SCC-4 Cells JF Anticancer Research JO Anticancer Res FD International Institute of Anticancer Research SP 4503 OP 4511 VO 29 IS 11 A1 TSAN-HUNG CHIU A1 WAN-WEN LAI A1 TE-CHUN HSIA A1 JAI-SING YANG A1 TUNG-YUAN LAI A1 PING-PING WU A1 CHIA-YU MA A1 CHIN-CHUNG YEH A1 CHIN-CHIN HO A1 HSU-FENG LU A1 W. GIBSON WOOD A1 JING-GUNG CHUNG YR 2009 UL http://ar.iiarjournals.org/content/29/11/4503.abstract AB Aloe-emodin, one of the anthraquinones, has been shown to have anticancer activity in different kinds of human cancer cell lines. Therefore, the purpose of this study was to investigate the anti-cancer effect of aloe-emodin on human tongue squamous carcinoma SCC-4 cells. The results indicated that aloe-emodin induced cell death through S-phase arrest and apoptosis in a dose- and time-dependent manner. Treatment with 30 μM of aloe-emodin led to S-phase arrest through promoted p53, p21 and p27, but inhibited cyclin A, E, thymidylate synthase and Cdc25A levels. Aloe-emodin promoted the release of apoptosis-inducing factor (AIF), endonuclease G (Endo G), pro-caspase-9 and cytochrome c from the mitochondria via a loss of the mitochondrial membrane potential (ΔΨm) which was associated with a increase in the ratio of B-cell lymphoma 2-associated X protein (Bax)/B cell lymphoma/leukemia-2 (Bcl-2) and activation of caspase-9 and -3. The free radical scavenger N-acetylcysteine (NAC) and caspase inhibitors markedly blocked aloe-emodin-induced apoptosis. Aloe-emodin thus induced apoptosis in the SCC-4 cells through the Fas/death-receptor, mitochondria and caspase cascade. Aloe-emodin could be a novel chemotherapeutic drug candidate for the treatment of human tongue squamous cancer in the future.