S-Allylcysteine modulates the expression of E-cadherin and inhibits the malignant progression of human oral cancer |
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| Authors: | Feng-Yao Tang En-Pei Isabel Chiang Jing-Gung Chung Hong-Zin Lee Chia-Yun Hsu |
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| Institution: | 1. Biomedical Science Laboratory, Department of Nutrition, China Medical University, Taichung 40402, Taiwan;2. Department of Biological Science and Technology, China Medical University, Taichung 40402, Taiwan;3. School of Pharmacy, China Medical University, Taichung 40402, Taiwan;1. Department of Human Pathology, University of Messina, Messina, Italy;2. Department of Chemical, Biological, Pharmaceutical, and Environmental Sciences, University of Messina, Messina, Italy;3. Lymphoma Service, Memorial Sloan Kettering Cancer Center, New York, NY;4. Universitätsklinik für Innere Medizin V, Hämatologie & Onkologie, Innsbruck, Austria;5. Department of Hematology and CBMT, Bolzano, Italy;2. Neurochemistry Laboratory, Division of Neurotoxicology, National Center for Toxicological Research/FDA, Jefferson, AR, USA;3. Departamento de Bioquímica y Biología Molecular, Facultad de Medicina, Instituto Maimónides de Investigación Biomédica de Córdoba (IMIBIC), Hospital Universitario Reina Sofia/Universidad de Córdoba, Cordoba, Spain;4. Red Temática de Investigación Cooperativa en Envejecimiento y Fragilidad (RETICEF), Spain;1. Department of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran;2. Neurophysiology Research Center, Shahed University, Tehran, Iran;3. Department of Physiology, School of Medicine, Shahed University, Tehran, Iran |
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| Abstract: | Oral cancer is a prevalent type of cancer in Asian countries. Several studies indicated that garlic extracts such as diallyl disulfide (DADS) and diallyl trisulfide (DATS) have anticancer effects. However, the inhibitory effects of water soluble garlic extracts, S-allylcysteine (SAC), on the malignant progression of oral cancer have not been studied well yet. Thus, the purpose of this study was to investigate the inhibitory effects of SAC on the proliferation and progression of human oral squamous cancer CAL-27 cells.In the present study, we demonstrated that SAC dose dependently inhibited the growth of human oral squamous cancer cells. Our results showed that SAC induced the expression of E-cadherin adhesion molecule. Immunocytochemical staining result also revealed that SAC could restore the distribution of E-cadherin molecule on cell membrane. We further demonstrated that SAC stabilized the adherent junction complex of E-cadherin/β-catenin in oral cancer cells. Treatment with the MAPK/MEK specific inhibitor, PD098059, could up-regulate the expression of E-cadherin molecule. Furthermore, SAC significantly inhibited the activation of MAPK/ERK signaling pathway. These findings were associated with the down-regulation of the SLUG repressor protein.In conclusion, our results indicated that SAC effectively inhibited the proliferation, up-regulated the expression of E-cadherin molecule and stabilized the E-cadherin/β-catenin adherent junction complex in human oral squamous cancer cells. The mechanism of action was in part through the suppression of MAPK/ERK signaling pathway and down-regulation of the SLUG repressor protein. |
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