國家衛生研究院 NHRI:Item 3990099045/10854
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    题名: CISD2 haploinsufficiency disrupts calcium homeostasis, causes nonalcoholic fatty liver disease, and promotes hepatocellular carcinoma
    作者: Shen, ZQ;Chen, YF;Chen, JR;Jou, YS;Wu, PC;Kao, CH;Wang, CH;Huang, YL;Chen, CF;Huang, TS;Shyu, YC;Tsai, SF;Kao, LS;Tsai, TF
    贡献者: Institute of Molecular and Genomic Medicine
    摘要: CISD2 is located within the chromosome 4q region frequently deleted in hepatocellular carcinoma (HCC). Mice with Cisd2 heterozygous deficiency develop a phenotype similar to the clinical manifestation of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH). Cisd2 haploinsufficiency causes a low incidence (20%) of spontaneous HCC and promotes HBV-associated and DEN-induced HCC; conversely, 2-fold overexpression of Cisd2 suppresses HCC in these models. Mechanistically, Cisd2 interacts with Serca2b and mediates its Ca(2+) pump activity via modulation of Serca2b oxidative modification, which regulates ER Ca(2+) uptake and maintains intracellular Ca(2+) homeostasis in the hepatocyte. CISD2 haploinsufficiency disrupts calcium homeostasis, causing ER stress and subsequent NAFLD and NASH. Hemizygous deletion and decreased expression of CISD2 are detectable in a substantial fraction of human HCC specimens. These findings substantiate CISD2 as a haploinsufficient tumor suppressor and highlights Cisd2 as a drug target when developing therapies to treat NAFLD/NASH and prevent HCC.
    日期: 2017-11-21
    關聯: Cell Reports. 2017 Nov 21;21(8):2198-2211.
    Link to: http://dx.doi.org/10.1016/j.celrep.2017.10.099
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=2211-1247&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000416216700016
    Cited Times(Scopus): https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85034806909
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