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 microM 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 (DeltaPsi(m)) 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.

PMID: 20032398 [PubMed − indexed for MEDLINE] Source: National Library of Medicine.