Allicin induces apoptosis in gastric cancer cells through activation of both extrinsic and intrinsic pathways

Abstract

Allicin is an active compound derived from garlic that has been shown tohave antitumor properties in vitro. The current study was designed toexplore the effects and the underlying mechanism of allicin on gastriccancer cells. The MTT assay was used to detect cell viability.Transmission electron microscopy, Rh123 and propidium iodide staining,Annexin V/FITC assay and the mitochondrial membrane potential were usedto assess for the presence of apoptosis. immunocytochemistry, Westernblot analysis, and Q-RT-PCR were used to detect gene expression. Wefound that allicin reduced cell viability in a dose- and time-dependentmanner, partly through induction of apoptosis in gastric cancer cells.At the molecular level, allicin induced cytochrome c release from themitochondria and increased caspase-3, -8, and -9 activation, withconcomitant upregulation of bax and fas expression in the tumor cells.Allicin treatment inhibited proliferation and induced apoptosis inSGC-7901 cancer cells. Both intrinsic mitochondrial and extrinsicFas/FasL-mediated pathways of apoptosis occur simultaneously in SGC-7901cells following allicin treatment. Data from the current studydemonstrated that allicin should be further investigated as a novelcancer preventive or therapeutic agent in control of gastric cancer,with potential uses in other tumor types.