Cytoglobin ameliorates the stemness of hepatocellular carcinoma via coupling oxidative-nitrosative stress signals.
作者： Jun Zhang , YuanYuan Pei , Wen Yang , WenXiu Yang , BoXin Chen
DOI: 10.1002/MC.22931
关键词:
摘要: Cancer stem cells (CSCs) account for tumor self-renewal and heterogeneity. Oxidative-nitrosative stress (ONS) is an independent etiologic factor throughout tumorigenesis. Emerging evidences indicated that the interaction of ONS with CSCs contributes to progression resistance chemoradiotherapy. Cytoglobin (Cygb) a member human hexacoordinate hemoglobin family acts as dynamic mediator redox homeostasis. We observed Cygb significantly deregulated in hepatocellular carcinoma (HCC) tissue its decrease aggravates growth liver cancer (LCSCs) increases subpopulation CD133(+) LCSCs. restoration inhibits HCC proliferation LCSC growth, decreases CD133 (+) LCSCs vitro. found absence promotes phenotypes PI3 K/AKT activation, whereas activation. Furthermore, exogenous antioxidants can eliminate inhibitory effect phenotypes, well Collectively, this study demonstrated cytoglobin functions suppressor targets at ONS-dependent manner. Thus, could be novel promising therapeutic strategy against aberrant ROS/RNS accumulation.
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