TFEB
自噬
溶酶体
细胞生物学
mTORC1型
自噬体
雷帕霉素的作用靶点
化学
PI3K/AKT/mTOR通路
生物发生
生物
生物化学
信号转导
基因
酶
细胞凋亡
作者
Zhenxing Li,Xu Wang,Zhichen Shi,Junting Xu,Jieru E. Lin,Dianlong Li,Xinpeng Zhang,Yuyin Li,Qian Zhao,Tao Li,Aipo Diao
标识
DOI:10.1139/bcb-2020-0570
摘要
Autophagy plays a key role in the metabolism of macromolecules via the degradative abilities of the lysosome. Transcription factor EB (TFEB) regulates autophagosome biogenesis and lysosome function, and promoting TFEB activity has emerged as a potential strategy for the treatment of metabolic disorders. Herein, we report that cetrimonium bromide (CTAB; a quaternary ammonium compound) promotes autophagy and lysosomal biogenesis by inducing the nuclear translocation of TFEB in hepatic cells. Knockdown of TFEB mediated by short hairpin RNA inhibits CTAB-induced autophagy and lysosomal biogenesis. Mechanistically, CTAB treatment inhibits the Akt-mTORC1 signaling pathway. Moreover, CTAB treatment significantly increases lipid metabolism in both palmitate- and oleate-treated HepG2 cells, and this increase was attenuated by knockdown of TFEB. Collectively, our results indicate that CTAB activates the autophagosome-lysosome pathway via inducing the nuclear translocation of TFEB by inhibiting the mTORC1 signaling pathway. These results add to the collective understanding of TFEB function and provide new insights into CTAB-mediated lipid metabolism.
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