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RISS 인기검색어
- 검색키워드
- 저자 : ( Anup Shrestha ) (검색결과 4 건)
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( Anup Shrestha ),( Pil Hoon Park ) 영남대학교 약품개발연구소 2016 영남대학교 약품개발연구소 연구업적집 Vol.26 No.-
Aims: Adiponectin has been shown to possess potent anti-oxidative properties in various experimental condi-tions, However, its anti-oxidative effects and underlying mechanisms have not been reported in liver cells, Herein, we investigated the effects of globular adiponectin (gAcrp) on LPS-stimulated reactive oxygen species (ROS) production and its mechanisms underlying in human hepatic cells (HepG2). Main methads: Intracellular ROS production was determined by fluorescence of 5-chloromethyl-2,7-dichlorodihydrofluorescein diacetate (CM-H2DCFDA). NADPH oxidase-dependent ROS formation was deter-mined by lucigenin-derived chemiluminescence. Messenger RNA expression level of target genes was deter-mined by quantitative RT-PCR and protein expression was measured by Western blot analysis. Key findings: LPS-induced increase in ROS production was prevented by pretreatment with gAcrp in HepG2 cells. Furthermore, gAcrp treatment suppressed LPS-induced activation of NADPH oxidase and increase in mRNA and protein expression of Nox-4. We also found that adiponectin increased expression of Fox03A and HO-1 and ab-lation of either of these genes partially restored suppression of LPS-induced ROS production and NADPH oxidase activation by gAcrp, indicating the vital role of Fox03A and HO-1 signaling in the inhibition ofROS production and NADPH oxidase activation by gAcrp. Significance: These results suggest that gAcrp prevents LPS-induced ROS production and NADPH oxidase activity in HepG2 cells via Fox03A and HO-1 signaling-dependent mechanisms. The present study demonstrated a sup-pressive effect of adiponeetin on ROS production in liver cells and presented a novel mechanism underlying sup-pression of ROS production by adiponectin.
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( Anup Shrestha ),( Saroj Nepal ),( Mijin Kim ),( Jae Hoon Chang ),( Sang Hyun Kim ),( Gil Saeng Jeong ),( Chul Ho Jeong ),( Gyu Hwan Park ),( Sunghee Jung ),( Jaecheong Lim ),( Eunha Cho ),( Soyoung 영남대학교 약품개발연구소 2016 영남대학교 약품개발연구소 연구업적집 Vol.26 No.-
Adiponeectin predominantly secreted from adipose tissue has exhibited potent anti- proliferative properties in cancer cells via modulating cell cycle and apoptosis, FoxO3A. a Forkhead box 0 member of the transcription factor. plays a critical role in modulating expression of genes involved In cell de:uh andlor SUrviV31. In this study. we investigated the role of FoxO3A signaling in and-cancer activities of adiponectin. Herein. we have shown that treaunent with globular adlponectln (gAcrp) Increases p27 but decreases cyclinD I expression In human hepatoma (HepG2) and breasr (MCF-7) cancer cells. Gene ablation of Fox03A prevented gAcrp-induced increase In p27 and decreased in cyelin 0 I expression. and further ameliorated cell cycle arrest by gAcrp.lndicating 3 critical role of FoxO3A in gAcrp-induced cell cycle arrest of cancer cells. Moreover, treatment with gAcrp also induced caspase-Jf7 activation and increased Fas ligand (Fasl) expression ln both HepG2 and MCF-7 cells. Transfecucn with FoxO3A siRNA inhibited gAcrp-induced caspase-3/7 activadon and Fasl expression. suggening that FoxO3A sigltaling also plays an lmportant role In gAcrp.induced apcptosis of cancer cells, We also found that gene silencing of AMPK prevented gAcrp-induced nuclear translocation of Fox03A in HepG2 and MCF-7 cells. In addition. suppression of AMPK also blocked gAcrp-lnduced cell cyele arrest and further attenuated gAcrp-induced caspase-3/7 activation, indICating that AMPK signaling plays a pivotal role in both gAcrp-lnduced cell cycle arrest and apoprosis via acting as an upstream S1gnalirlg of Fox03A Taken together. our firldings demonstrated that AMPK/Fox03A axis plays a cardinal role in anu-protlferanve effect of adiponecun in cancer cells.
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( Saroj Nepal ),( Anup Shrestha ),( Pil Hoon Park ) 영남대학교 약품개발연구소 2016 영남대학교 약품개발연구소 연구업적집 Vol.26 No.-
Adiponectin and leptin, both produced from adipose tissue, cause cell cycle arrest and progression, re-spectively in cancer cells. Ubiquitin specific protease-2 (USP-2). a deubiquitinating enzyme, is known to impair proteasorne-induced degradation of cyelin D1, a critical cell cycle regulator. Herein, we investi-gated the effects of these adipokines on USP-2 expression and its potential role in the modulation of cell cycle. Treatment with globular adiponectin (gAcrp) decreased, whereas leptin increased USP-2 expres-sion both in human hepatoma and breast cancer cells. In addition, overexpression or gene silencing of USP-2 affected cyelin D1 expression and cell cycle progression/arrest by adipokines. Adiponectin and leptin also modulated in vitro proteasomal activity, which was partially dependent on USP-2 expression. Taken together. our results reveal that modulation of USP-2 expression plays a crucial role in cell cycle regu-lation by adipokines. Thus. USP-2 would be a promising therapeutic target for the modulation of cancer cell growth by adipokines.
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