Journal
ONCOLOGY LETTERS
Volume 8, Issue 6, Pages 2591-2596Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/ol.2014.2579
Keywords
human colorectal carcinoma cells; SW620; p53; S-allylmercaptocysteine; c-Jun N-terminal kinase; signal pathway; p38
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S-allylmercaptocysteine (SAMC) is an active compound that is derived from garlic and has been demonstrated to possess antitumor properties in vitro. The present study aimed to investigate the effect of SAMC and determine the underlying mechanism of this effect on human colorectal carcinoma cells. The SW620 cells were cultured with various concentrations of SAMC and cell viability was detected using an MTT assay. Analysis of apoptosis was performed using terminal deoxynucleotidyl-transferase-mediated deoxyuridine triphosphate nick end labeling. The c-Jun N-terminal kinase (JNK) and p38 mitogen activated protein kinase (p38) signaling pathways were investigated by polymerase chain reaction. SAMC was observed to reduce cell viability in a dose- and time-dependent manner, partially through the induction of apoptosis in human colorectal carcinoma cells. At the molecular level, SAMC induces apoptosis through JNK and p38 signaling pathways, increasing tumor protein p53 (p53) and Box activation in the SW620 cells. The most effective concentration of SAMC for the induction of SW620 cell apoptosis was found to be 400 mu M, which was confirmed through cell viability assays and apoptosis analysis. The current study indicated that SAMC inhibits cell proliferation and induces apoptosis of SW620 cells via the JNK and p38 pathways. The results from the current study demonstrated that SAMC must be further investigated as a novel preventive or therapeutic agent for the treatment of colorectal carcinoma, and potentially for use in other tumor types.
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