Sulforaphane suppresses oral cancer cell migration by regulating cathepsin S expression
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Chang-Tai Chen1,2,*, Ming-Ju Hsieh3,4,5,*, Yi-Hsien Hsieh6, Min-Chieh Hsin3, Yi-Ting Chuang3, Shun-Fa Yang3,7, Jia-Sin Yang3,7 and Chiao-Wen Lin1,2,8
1Institute of Oral Sciences, Chung Shan Medical University, Taichung, Taiwan
2School of Dentistry, Chung Shan Medical University, Taichung, Taiwan
3Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan
4Cancer Research Center, Changhua Christian Hospital, Changhua, Taiwan
5Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan
6Institute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, Taiwan
7Department of Medical Research, Chung Shan Medical University Hospital, Taichung, Taiwan
8Department of Dentistry, Chung Shan Medical University Hospital, Taichung, Taiwan
*These authors contributed equally to this work
Chiao-Wen Lin, email: [email protected]
Jia-Sin Yang, email: [email protected]
Keywords: sulforaphane; cathepsin S; LC3; oral cancer; migration
Received: November 09, 2017 Accepted: February 28, 2018 Published: April 03, 2018
Sulforaphane has been demonstrated to exert numerous biological effects, such as neuroprotective, anti-inflammatory, and anticancer effects. However, the detailed effects of sulforaphane on human oral cancer cell migration and the underlying mechanisms remain unclear. In this study, we observed that sulforaphane attenuated SCC-9 and SCC-14 cell motility and invasiveness by reducing cathepsin S expression. Moreover, sulforaphane increased microtubule-associated protein 1 light chain 3 (LC3) conversion, and the knockdown of LC3 by siRNA increased cell migration ability. Regarding the mechanism, sulforaphane inhibited the cell motility of oral cancer cells through the extracellular signal-regulated kinase (ERK) pathway, which in turn reversed cell motility. In conclusion, sulforaphane suppress cathepsin S expression by inducing autophage through ERK signaling pathway. Thus, cathepsin S and LC3 may be new targets for oral cancer treatment.
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