Abstract:
:Adiponectin blocks hepatocellular carcinoma (HCC) progression by inducing cell apoptosis through the modulation of C-Jun N-terminal kinase and mammalian target of rapamycin. However, the precise upstream signaling pathways or molecules remain elusive. In the present study, we analyzed the role of antioxidant protein thioredoxin (Trx) in adiponectin-induced apoptosis in HCC. Adiponectin treatment decreased the viabilities of both HepG2 and Huh7 HCC cells accompanied by increased accumulation of intracellular reactive oxygen species, as evidenced by 2',7'-dichlorodihydrofluorescein diacetate staining. Pretreatment of these cells with the deoxidant N-acetylcysteine blocked the inhibitory effect of adiponectin. Levels of Trx2 protein in both HCC cells were significantly decreased, and the level of Trx1 was significantly inhibited in Huh7 cells while unchanged in HepG2 cells. However, the redox state of Trx1 was altered from reduced to the oxidized form following adiponectin treatment in HepG2 cells. Overexpression of both Trx proteins rescued adiponectin-induced cell apoptosis, whereas mutated Trx proteins were less effective. Further analysis suggested that both ASK1 and JNK signaling are involved in this process. Trx1 and Trx2 proteins also manifested protective effects on HCC cells in response to adiponectin treatment in a xenograft tumor model. Furthermore, high levels of Trx proteins and low adiponectin expression levels were found in primary human HCC samples compared with paracancerous tissues. These results suggest that Trx proteins play important roles in mediating adiponectin-induced HCC cell apoptosis, thus providing new insights into the pathogenesis of HCC and identifying adiponectin and Trx proteins as potential combinational therapeutic targets for the treatment of HCC.
journal_name
Biochem Pharmacoljournal_title
Biochemical pharmacologyauthors
Xing SQ,Zhang CG,Yuan JF,Yang HM,Zhao SD,Zhang Hdoi
10.1016/j.bcp.2014.12.001subject
Has Abstractpub_date
2015-01-15 00:00:00pages
221-31issue
2eissn
0006-2952issn
1873-2968pii
S0006-2952(14)00696-0journal_volume
93pub_type
杂志文章abstract::Net cadmium uptake in the isolated perfused rat liver was half-maximal at 5 microM, and the maximal rate of uptake was 22 nmoles/min per gram liver wet weight. Uptake was augmented when a permeable thiol, dithioerythritol, was infused, whereas it was restricted when glutathione as a nonpermeable thiol or also when bov...
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journal_title:Biochemical pharmacology
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journal_title:Biochemical pharmacology
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doi:10.1016/j.bcp.2004.12.004
更新日期:2005-03-15 00:00:00
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pub_type: 杂志文章
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