YI-HSIEN HSIEHSHUN-FA YANGCHIAO-WEN LIN2026-10-162026-10-162018-04-01Pure ID: 15152642Pure UUID: db97d4cb-eb4f-49f8-985c-9b8449c3780d10.18632/oncotarget.24786https://www.scopus.com/pages/publications/85044827154https://scholars.csmu.edu.tw/handle/123456789/25893Sulforaphane 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.12enjournal article