%0 Journal Article
%T GCLC、GCLM在肿瘤中的作用研究进展概述<br>Review on the Research Progress of GCLC and GCLM in Tumors
%A 达德转
%A 潘志昂
%A 党春艳
%A 李红玲
%J World Journal of Cancer Research
%P 1-6
%@ 2164-9057
%D 2022
%I Hans Publishing
%R 10.12677/WJCR.2022.121001
%X 我国肿瘤发病率与死亡率居高，以乳腺癌、肺癌为代表的恶性肿瘤的诊治面临巨大挑战。氧化应激是指由于活性物质的产生或氧化还原系统代偿能力有限使得细胞内氧化还原状态被破坏的一种病理过程。研究表明氧化应激与肿瘤中氧化应激水平多处于失衡状态并与恶性肿瘤发生发展密切相关。谷胱甘肽(glutathione, GSH)在肺癌、结直肠癌等多种肿瘤中异常表达且与氧化应激失衡相关。另外参与合成GSH的关键酶谷氨酸半胱氨酸连接酶(glutamate cysteine ligase, GCL)及其亚基也受到很大关注，他们可能是造成恶性肿瘤中GSH合成紊乱及氧化应激失衡的重要原因，并在不同肿瘤中发挥促癌或抑癌的作用。但是GCL及其亚基与肿瘤发生发展的关系、与患者临床病理特征的关系尚未系统阐述，该文就GCL及其亚基在肿瘤中的表达及其意义进行综述。<br />
The incidence and mortality of cancer are high in China, but the diagnosis and treatment of malignant tumors represented by breast cancer and lung cancer are facing great challenges. Oxidative stress refers to a pathological process in which the redox state in cells is destroyed due to the production of active substances or the limited compensatory capacity of REDOX system. Studies have shown that oxidative stress is often unbalanced with the level of oxidative stress in tumors and is closely related to the occurrence and development of malignant tumors. Glutathione (GSH) is abnormally expressed in lung cancer, colorectal cancer and other tumors and is associated with oxidative stress imbalance. In addition, glutamate cysteine ligase (GCL) and its subunits, a key enzyme involved in the synthesis of GSH, have also attracted great attention, which may be an important cause of GSH synthesis disorder and oxidative stress imbalance in malignant tumors, and play a role in promoting or inhibiting cancer in different tumors. However, the relationship between GCL and its subunits and tumor development and clinicopathological features of patients has not been systematically described. Therefore, this paper reviews the expression and significance of GCL and its subunits in tumors.
%K 谷氨酸半胱氨酸连接酶，谷氨酸半胱氨酸催化亚基，谷氨酸半胱氨酸修饰亚基，氧化应激，肿瘤<br>GCL
%K GCLC
%K GCLM
%K ROS
%K Tumors
%U http://www.hanspub.org/journal/PaperInformation.aspx?PaperID=47850