萝卜硫素通过调节组织蛋白酶S的表达来抑制口腔癌细胞的迁移。
Sulforaphane suppresses oral cancer cell migration by regulating cathepsin S expression.
作者信息
Chen Chang-Tai, Hsieh Ming-Ju, Hsieh Yi-Hsien, Hsin Min-Chieh, Chuang Yi-Ting, Yang Shun-Fa, Yang Jia-Sin, Lin Chiao-Wen
机构信息
Institute of Oral Sciences, Chung Shan Medical University, Taichung, Taiwan.
School of Dentistry, Chung Shan Medical University, Taichung, Taiwan.
出版信息
Oncotarget. 2018 Apr 3;9(25):17564-17575. doi: 10.18632/oncotarget.24786.
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.
已证明萝卜硫素具有多种生物学效应,如神经保护、抗炎和抗癌作用。然而,萝卜硫素对人口腔癌细胞迁移的具体影响及其潜在机制仍不清楚。在本研究中,我们观察到萝卜硫素通过降低组织蛋白酶S的表达来减弱SCC - 9和SCC - 14细胞的运动性和侵袭性。此外,萝卜硫素增加了微管相关蛋白1轻链3(LC3)的转化,并且通过小干扰RNA敲低LC3可增加细胞迁移能力。关于其机制,萝卜硫素通过细胞外信号调节激酶(ERK)途径抑制口腔癌细胞的运动性,进而逆转细胞运动性。总之,萝卜硫素通过ERK信号通路诱导自噬来抑制组织蛋白酶S的表达。因此,组织蛋白酶S和LC3可能是口腔癌治疗的新靶点。