蘿蔔硫素(Sulforaphane)已被證實可以參與在許多生物反應，如神經保護、抗發炎作用、以及抗癌反應等等。然而，蘿蔔硫素對於人類口腔癌細胞的轉移以及其潛在機制並不清楚。在本篇研究中，我們觀察到蘿蔔硫素可以透過降低組織蛋白?S(cathepsin S)的表現來降低口腔癌細胞株SCC-9與SCC-14的移動性與侵襲性。此外，蘿蔔硫素增加了維管相關蛋白1輕鏈3(light chain 3, LC3)的轉換，我們也使用了LC3的siRNA將LC3的基因下調，使得細胞的移動力增加。關於此機制，蘿蔔硫素是透過細胞外信號調節激?extracellular signal-regulated kinase, ERK）路徑來抑制口腔癌細胞的移動性，將其抑制亦可反轉其細胞移動性。總之，蘿蔔硫素透過細胞外信號調節激?誘導細胞自噬作用進而抑制組織蛋白?S的表現；因此組織蛋白?S以及LC3也許可以成為口腔癌治療上的新標靶目標。
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 autophagy through ERK signaling pathway. Thus, cathepsin S and LC3 may be new targets for oral cancer treatment.
