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人恶性黑色素瘤中 GLO1 的过表达。

GLO1 overexpression in human malignant melanoma.

机构信息

Department of Pharmacology and Toxicology, College of Pharmacy and Arizona Cancer Center, University of Arizona, Tucson, USA.

出版信息

Melanoma Res. 2010 Apr;20(2):85-96. doi: 10.1097/CMR.0b013e3283364903.

Abstract

Glyoxalase I [lactoylglutathione lyase (EC 4.4.1.5) encoded by GLO1] is a ubiquitous cellular defense enzyme involved in the detoxification of methylglyoxal, a cytotoxic byproduct of glycolysis. Accumulative evidence suggests an important role of GLO1 expression in protection against methylglyoxal-dependent protein adduction and cellular damage associated with diabetes, cancer, and chronological aging. On the basis of the hypothesis that GLO1 upregulation may play a functional role in glycolytic adaptations of cancer cells, we examined GLO1 expression status in human melanoma tissue. Quantitative reverse transcription polymerase chain reaction analysis of a cDNA tissue array containing 40 human melanoma tissues (stages III and IV) and 13 healthy controls revealed pronounced upregulation of GLO1 expression at the mRNA level. Immunohistochemical analysis of a melanoma tissue microarray confirmed upregulation of glyoxalase I protein levels in malignant melanoma tissue versus healthy human skin. Consistent with an essential role of GLO1 in melanoma cell defense against methylglyoxal cytotoxicity, siRNA interference targeting GLO1-expression (siGLO1) sensitized A375 and G361 human metastatic melanoma cells towards the antiproliferative, apoptogenic, and oxidative stress-inducing activity of exogenous methylglyoxal. Protein adduction by methylglyoxal was increased in siGLO1-transfected cells as revealed by immunodetection using a monoclonal antibody directed against the major methylglyoxal-derived epitope argpyrimidine that detected a single band of methylglyoxal-adducted protein in human LOX, G361, and A375 total cell lysates. Using two-dimensional proteomics followed by mass spectrometry the methylglyoxal-adducted protein was identified as heat shock protein 27 (Hsp27; HSPB1). Taken together, our data suggest a function of GLO1 in the regulation of detoxification and target adduction by the glycolytic byproduct methylglyoxal in malignant melanoma.

摘要

一氧戊二醛酶 I [乳糖酰谷胱甘肽裂合酶(EC 4.4.1.5),由 GLO1 编码] 是一种普遍存在的细胞防御酶,参与甲基乙二醛的解毒,甲基乙二醛是糖酵解的细胞毒性副产物。累积的证据表明 GLO1 表达在保护甲基乙二醛依赖性蛋白质加合物和与糖尿病、癌症和生物钟衰老相关的细胞损伤方面发挥着重要作用。基于 GLO1 上调可能在癌细胞糖酵解适应中发挥功能作用的假设,我们检查了人黑色素瘤组织中的 GLO1 表达状态。包含 40 个人黑色素瘤组织(III 和 IV 期)和 13 个健康对照的 cDNA 组织阵列的定量逆转录聚合酶链反应分析显示,GLO1 在 mRNA 水平上的表达明显上调。对黑色素瘤组织微阵列的免疫组织化学分析证实,与健康人皮肤相比,恶性黑色素瘤组织中糖氧合酶 I 蛋白水平上调。与 GLO1 在黑色素瘤细胞防御甲基乙二醛细胞毒性中的重要作用一致,针对 GLO1 表达的 siRNA 干扰(siGLO1)使 A375 和 G361 人转移性黑色素瘤细胞对细胞外甲基乙二醛的抗增殖、促凋亡和氧化应激诱导活性敏感。在用针对主要甲基乙二醛衍生表位精氨酸嘧啶的单克隆抗体进行免疫检测时,在用 siGLO1 转染的细胞中,蛋白质加合物由甲基乙二醛增加,该抗体检测到人 LOX、G361 和 A375 总细胞裂解物中单个甲基乙二醛加合物蛋白条带。使用二维蛋白质组学随后进行质谱分析,鉴定出甲基乙二醛加合物蛋白为热休克蛋白 27(Hsp27;HSPB1)。总之,我们的数据表明 GLO1 在调节恶性黑色素瘤中糖酵解副产物甲基乙二醛的解毒和靶标加合物方面发挥作用。

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