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Identification of biomarkers associated with the development of hepatocellular carcinoma in CuZn superoxide dismutase deficient mice.在铜锌超氧化物歧化酶缺陷小鼠中鉴定与肝细胞癌发生相关的生物标志物。
Proteomics. 2007 Jun;7(12):2121-9. doi: 10.1002/pmic.200601011.
2
CuZnSOD deficiency leads to persistent and widespread oxidative damage and hepatocarcinogenesis later in life.铜锌超氧化物歧化酶缺乏会导致持续广泛的氧化损伤，并在生命后期引发肝癌。
Oncogene. 2005 Jan 13;24(3):367-80. doi: 10.1038/sj.onc.1208207.
3
Sexual dimorphism in LEC rat liver: suppression of carbonic anhydrase III by copper accumulation during hepatocarcinogenesis.LEC大鼠肝脏中的性别二态性：肝癌发生过程中铜积累对碳酸酐酶III的抑制作用。
Biomed Res. 2011 Apr;32(2):111-7. doi: 10.2220/biomedres.32.111.
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Suppressive role of regucalcin in liver cell proliferation: involvement in carcinogenesis.Regucalcin 在肝细胞增殖中的抑制作用：与癌变的关系。
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CuZn-SOD deficiency causes ApoB degradation and induces hepatic lipid accumulation by impaired lipoprotein secretion in mice.铜锌超氧化物歧化酶缺乏导致载脂蛋白B降解，并通过损害小鼠脂蛋白分泌诱导肝脏脂质蓄积。
J Biol Chem. 2006 Oct 20;281(42):31713-9. doi: 10.1074/jbc.M603422200. Epub 2006 Aug 20.
6
Knockout of SOD1 alters murine hepatic glycolysis, gluconeogenesis, and lipogenesis.SOD1 基因敲除改变了小鼠肝脏的糖酵解、糖异生和脂生成。
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Copper, zinc-superoxide dismutase protein but not mRNA is lower in copper-deficient mice and mice lacking the copper chaperone for superoxide dismutase.在缺铜小鼠和缺乏超氧化物歧化酶铜伴侣蛋白的小鼠中，铜锌超氧化物歧化酶蛋白水平降低，但mRNA水平未降低。
Exp Biol Med (Maywood). 2003 Sep;228(8):959-66. doi: 10.1177/153537020322800812.
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Isoaspartate, carbamoyl phosphate synthase-1, and carbonic anhydrase-III as biomarkers of liver injury.异天冬氨酸、氨甲酰磷酸合成酶-1和碳酸酐酶-III作为肝损伤的生物标志物。
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Role of superoxide-nitric oxide interactions in the accelerated age-related loss of muscle mass in mice lacking Cu,Zn superoxide dismutase.缺乏 Cu,Zn 超氧化物歧化酶的小鼠中超氧化物-一氧化氮相互作用在加速与年龄相关的肌肉质量损失中的作用。
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Carbonic anhydrase III promotes transformation and invasion capability in hepatoma cells through FAK signaling pathway.碳酸酐酶III通过FAK信号通路促进肝癌细胞的转化和侵袭能力。
Mol Carcinog. 2008 Dec;47(12):956-63. doi: 10.1002/mc.20448.

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Transcriptomic Analysis of the Liver Redox Response During Food-Anticipatory Activity Under a Time-Restricted Feeding Protocol in Rats.大鼠限时进食方案下食物预期活动期间肝脏氧化还原反应的转录组学分析
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Regucalcin Is a Potential Regulator in Human Cancer: Aiming to Expand into Cancer Therapy.调钙素是人类癌症中的一种潜在调节因子：旨在拓展至癌症治疗领域。
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Double Knockout of Peroxiredoxin 4 (Prdx4) and Superoxide Dismutase 1 (Sod1) in Mice Results in Severe Liver Failure.小鼠过氧化物酶 4（Prdx4）和超氧化物歧化酶 1（Sod1）双重敲除导致严重肝衰竭。
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Expression of liver fatty acid binding protein in hepatocellular carcinoma.肝脏脂肪酸结合蛋白在肝细胞癌中的表达
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iTRAQ-based proteomic analysis of hepatic tissues from patients with hepatitis B virus-induced acute-on-chronic liver failure.基于iTRAQ的乙型肝炎病毒所致慢加急性肝衰竭患者肝组织蛋白质组学分析
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Hepatic and renal expression of senescence marker protein-30 and its biological significance.衰老标记蛋白-30的肝脏和肾脏表达及其生物学意义。
J Gastroenterol Hepatol. 1998 Sep;13(S1):S124-S131. doi: 10.1111/jgh.1998.13.s1.124.
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Vitamin C. Biosynthesis, recycling and degradation in mammals.维生素C。哺乳动物中的生物合成、循环利用与降解
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Detection of protein carbonyls in aging liver tissue: A fluorescence-based proteomic approach.衰老肝脏组织中蛋白质羰基的检测：一种基于荧光的蛋白质组学方法。
Mech Ageing Dev. 2006 Nov;127(11):849-61. doi: 10.1016/j.mad.2006.08.006. Epub 2006 Sep 26.
4
Overexpression of regucalcin enhances glucose utilization and lipid production in cloned rat hepatoma H4-II-E cells: Involvement of insulin resistance.调节钙素的过表达增强克隆大鼠肝癌H4-II-E细胞中的葡萄糖利用和脂质生成：与胰岛素抵抗有关。
J Cell Biochem. 2006 Dec 15;99(6):1582-92. doi: 10.1002/jcb.21005.
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Senescence marker protein 30 functions as gluconolactonase in L-ascorbic acid biosynthesis, and its knockout mice are prone to scurvy.衰老标记蛋白30在L-抗坏血酸生物合成中作为葡糖酸内酯酶发挥作用，其基因敲除小鼠易患坏血病。
Proc Natl Acad Sci U S A. 2006 Apr 11;103(15):5723-8. doi: 10.1073/pnas.0511225103. Epub 2006 Apr 3.
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Antioxidative function of L-FABP in L-FABP stably transfected Chang liver cells.L-FABP稳定转染的Chang肝细胞中L-FABP的抗氧化功能
Hepatology. 2005 Oct;42(4):871-9. doi: 10.1002/hep.20857.
7
Suppressive effect of regucalcin on cell differentiation and mineralization in osteoblastic MC3T3-E1 cells.调钙素对成骨细胞MC3T3-E1细胞分化和矿化的抑制作用。
J Cell Biochem. 2005 Oct 15;96(3):543-54. doi: 10.1002/jcb.20524.
8
Overexpression of regucalcin suppresses cell proliferation in cloned rat hepatoma H4-II-E cells: involvement of intracellular signaling factors and cell cycle-related genes.调节钙素的过表达抑制克隆大鼠肝癌H4-II-E细胞的增殖：细胞内信号因子和细胞周期相关基因的参与
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Glutathione transferases.谷胱甘肽转移酶
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10
Overexpression of alpha enolase in hepatitis C virus-related hepatocellular carcinoma: association with tumor progression as determined by proteomic analysis.α-烯醇化酶在丙型肝炎病毒相关肝细胞癌中的过表达：蛋白质组学分析确定其与肿瘤进展的关联
Proteomics. 2005 Apr;5(6):1686-92. doi: 10.1002/pmic.200401022.

在铜锌超氧化物歧化酶缺陷小鼠中鉴定与肝细胞癌发生相关的生物标志物。

Identification of biomarkers associated with the development of hepatocellular carcinoma in CuZn superoxide dismutase deficient mice.

作者信息

Elchuri Sailaja, Naeemuddin Mohammed, Sharpe Orr, Robinson William H, Huang Ting-Ting

机构信息

Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA, USA.

出版信息

Proteomics. 2007 Jun;7(12):2121-9. doi: 10.1002/pmic.200601011.

DOI:10.1002/pmic.200601011
PMID:17514684
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2729784/
Abstract

To identify biomarkers associated with the development of hepatocellular carcinoma (HCC) in CuZn superoxide dismutase (CuZnSOD, Sod1) deficient mice, 2-DE followed by MS analysis was carried out with liver samples obtained from 18-month-old Sod1-/- and +/+ mice. The intracellular Ca binding protein, regucalcin (RGN), showed a divergent alteration in Sod1-/- samples. Whereas elevated RGN levels were observed in -/- samples with no obvious neoplastic changes, marked reduction in RGN was observed in -/- samples with fully developed HCC. GST mu1 (GSTM1), on the other hand, showed a significant increase only in the neoplastic regions obtained from Sod1-/- livers. No change in GSTM1 was observed in the surrounding normal tissues. Marked reduction was observed in two intracellular lipid transporters, fatty acid binding protein 1 (FABP1) and major urinary protein 11 and 8 (MUP 11&8), in Sod1-/- samples. Analysis of additional samples at 18-22 months of age showed a three-fold increase in enolase activities in Sod1-/- livers. Consistent with previous findings, carbonic anhydrase 3 (CAIII) levels were significantly reduced in Sod1-/- samples, and immunohistochemical analysis revealed that the reduction was not homogenous throughout the lobular structure in the liver.

摘要

为了鉴定与铜锌超氧化物歧化酶（CuZnSOD，Sod1）缺陷小鼠肝细胞癌（HCC）发生相关的生物标志物，对18月龄Sod1 - / - 和 + / + 小鼠的肝脏样本进行了二维凝胶电泳（2-DE）及随后的质谱分析。细胞内钙结合蛋白调节钙素（RGN）在Sod1 - / - 样本中呈现出不同的变化。在没有明显肿瘤变化的 - / - 样本中观察到RGN水平升高，而在HCC完全发展的 - / - 样本中则观察到RGN显著降低。另一方面，谷胱甘肽S-转移酶mu1（GSTM1）仅在取自Sod1 - / - 肝脏的肿瘤区域显示出显著增加。在周围正常组织中未观察到GSTM1的变化。在Sod1 - / - 样本中，两种细胞内脂质转运蛋白脂肪酸结合蛋白1（FABP1）和主要尿蛋白11和8（MUP 11&8）显著降低。对18 - 22月龄的额外样本分析显示，Sod1 - / - 肝脏中烯醇化酶活性增加了三倍。与先前的研究结果一致，Sod1 - / - 样本中碳酸酐酶3（CAIII）水平显著降低，免疫组织化学分析表明这种降低在肝脏小叶结构中并非均匀分布。