Molecular basis and current strategies of therapeutic arginine depletion for cancer

被引：84

作者：

Fultang, Livingstone ^{[1
]}

Vardon, Ashley ^{[1
]}

De Santo, Carmela ^{[1
]}

Mussai, Francis ^{[1
]}

机构：

[1] Univ Birmingham, Inst Immunol & Immunotherapy, Birmingham, W Midlands, England

来源：

INTERNATIONAL JOURNAL OF CANCER | 2016年 / 139卷 / 03期

基金：

英国医学研究理事会;

关键词：

arginine deprivation; recombinant human arginase; arginine deiminase; ARGININOSUCCINATE SYNTHETASE EXPRESSION; AMINO-ACID SUFFICIENCY; HUMAN ARGINASE; CELL-DEATH; DEPRIVATION; TRANSPORTER; METABOLISM; DEIMINASE; AUTOPHAGY; KINASE;

D O I：

10.1002/ijc.30051

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Renewed interest in the use of therapeutic enzymes combined with an improved knowledge of cancer cell metabolism, has led to the translation of several arginine depletion strategies into early phase clinical trials. Arginine auxotrophic tumors are reliant on extracellular arginine, due to the downregulation of arginosuccinate synthetase or ornithine transcarbamylase-key enzymes for intracellular arginine recycling. Engineered arginine catabolic enzymes such as recombinant human arginase (rhArg1- PEG) and arginine deiminase (ADI-PEG) have demonstrated cytotoxicity against arginine auxotrophic tumors. In this review, we discuss the molecular events triggered by extracellular arginine depletion that contribute to tumor cell death.

引用

页码：501 / 509

页数：9

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