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Guan Feng,Ding Youming,He Yikang,Li Lu,Yang Xinyu,Wang Changhua,Hu Mingbai 대한약리학회 2022 The Korean Journal of Physiology & Pharmacology Vol.26 No.6
It has been demonstrated that APPL1 (adaptor protein, phosphotyrosine interacting with PH domain and leucine zipper 1) is involved in the regulation of several growth-related signaling pathways and thus closely associated with the development and progression of some cancers. Diallyl trisulfide (DAT), a garlic-derived bioactive compound, exerts selective cytotoxicity to various human cancer cells through interfering with pro-survival signaling pathways. However, whether and how DAT affects survival of human hepatocellular carcinoma (HCC) cells remain unclear. Herein, we tested the hypothesis of the involvement of APPL1 in DAT-induced cytotoxicity in HCC HepG2 cells. We found that Lys 63 (K63)-linked polyubiquitination of APPL1 was significantly decreased whereas phosphorylation of APPL1 at serine residues remained unchanged in DAT-treated HepG2 cells. Compared with wild-type APPL1, overexpression of APPL1 K63R mutant dramatically increased cell apoptosis and mitigated cell survival, along with a reduction of phosphorylation of STAT3, Akt, and Erk1/2. In addition, DAT administration markedly reduced protein levels of intracellular TNF receptor-associated factor 6 (TRAF6). Genetic inhibition of TRAF6 decreased K63-linked polyubiquitination of APPL1. Moreover, the cytotoxicity impacts of DAT on HepG2 cells were greatly attenuated by overexpression of wild-type APPL1. Taken together, these results suggest that APPL1 polyubiquitination probably mediates the inhibitory effects of DAT on survival of HepG2 cells by modulating STAT3, Akt, and Erk1/2 pathways.
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( Meng Li ),( Jiexia Ding ),( Xingyong Wan ),( Xi Jin ),( Shaohua Chen ),( Chaohui Yu ),( Youming Li ) 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1
Background: The mitochondrial enzyme 3-mercaptopyruvate sulfurtransferase (MPST) is a source of endogenous hydrogen sul.de (H2S), a gaseous signaling molecule implicated in a wide range of physiological processes. The mechanisms of pathogenesis underlying nonalcoholic fatty liver disease (NAFLD) remain unclear. The possible role of MPST in the development of NAFLD has never been investigated. Methods: The NAFLD cell model was established by treating L02 cells with free fatty acid (FFA) overload. A variety of cellular and molecular approaches were used to study the effects of MPST on hepatic steatosis, oxidative stress and inflammation involved in NAFLD. Results: After culturing L02 cells by FFA for 24h, we detected the increased protein level of MPST. MPST knockdown in L02 cells resulted in a marked decrease of lipid accumulation and downregulation of SREBP-1 pathway and melioration of oxdiative stress, embodied in decreased level of H2O2, MDA and IL-6, meanwhile, increased levels of ATP and MMP. Unexpectedly, we observed a significantly increased level of H2S after knockdown of MPST. And the expression of CSE was enhanced when the MPST was decreased. When the level of H2S was decreased, the TG and H2O2 content within FFA-induced hepatocytes were greatly raised. Meanwhile, we demonstrated the reversed expression of SREBP-1/ ACC pathway with the reduced level of H2S. Conclusions: We showed that MPST knockdown could stimulate the compensatory process of CSE, causing the increasing of H2S which is recently considered as a novel antioxidant gas. The increased endogenous H2S could improve hepatocyte steatosis and partly improve the process of oxidative stress and in. ammatory state of steatosis hepatocytes. MPST is implicated in NAFLD via its important H2S metabolism. It provided new insight into the pathogenic mechanisms of NAFLD, pointing to potential target for therapeutic strategy.
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