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 metastasis 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. Mechanistically, sulforaphane inhibited the cell motility of cervical cells through the extracellular signal-regulated kinase (ERK1/2) pathway, and blocking of the ERK1/2 pathway reversed autophagy-mediated cell motility and CTSS inhibition. In conclusion, sulforaphane exhibits antimetastatic activity against oral cancer cells by repressing cathepsin S through the ERK1/2 signaling pathway. Thus, cathepsin S and LC3 may be new targets for oral cancer treatment.

Citation Format: Chiao-Wen Lin, Chang-Tai Chen, Shun-Fa Yang. Sulforaphane suppresses metastasis via autophagic degradation of cathepsin S in oral cancer cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 4197.