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葡萄糖转运蛋白:子宫内膜癌治疗敏感性的重要调节因子。

Glucose transporters: Important regulators of endometrial cancer therapy sensitivity.

作者信息

Zhang Xing, Lu Jia-Jing, Abudukeyoumu Ayitila, Hou Ding-Yu, Dong Jing, Wu Jiang-Nan, Liu Li-Bing, Li Ming-Qing, Xie Feng

机构信息

Medical Center of Diagnosis and Treatment for Cervical and Intrauterine Diseases, Obstetrics and Gynecology Hospital of Fudan University, Shanghai, China.

Laboratory for Reproductive Immunology, Hospital of Obstetrics and Gynecology, Shanghai Medical School, Fudan University, Shanghai, China.

出版信息

Front Oncol. 2022 Aug 5;12:933827. doi: 10.3389/fonc.2022.933827. eCollection 2022.

Abstract

Glucose is of great importance in cancer cellular metabolism. Working together with several glucose transporters (GLUTs), it provides enough energy for biological growth. The main glucose transporters in endometrial cancer (EC) are Class 1 (GLUTs 1-4) and Class 3 (GLUTs 6 and 8), and the overexpression of these GLUTs has been observed. Apart from providing abundant glucose uptake, these highly expressed GLUTs also participate in the activation of many crucial signaling pathways concerning the proliferation, angiogenesis, and metastasis of EC. In addition, overexpressed GLUTs may also cause endometrial cancer cells (ECCs) to be insensitive to hormone therapy or even resistant to radiotherapy and chemoradiotherapy. Therefore, GLUT inhibitors may hopefully become a sensitizer for EC precision-targeted therapies. This review aims to summarize the expression regulation, function, and therapy sensitivity of GLUTs in ECCs, aiming to provide a new clue for better diagnosis and treatment of EC.

摘要

葡萄糖在癌细胞代谢中至关重要。它与多种葡萄糖转运蛋白(GLUTs)协同作用,为生物生长提供足够的能量。子宫内膜癌(EC)中的主要葡萄糖转运蛋白是1类(GLUTs 1 - 4)和3类(GLUTs 6和8),并且已观察到这些GLUTs的过表达。除了提供丰富的葡萄糖摄取外,这些高表达的GLUTs还参与许多与EC增殖、血管生成和转移相关的关键信号通路的激活。此外,过表达的GLUTs还可能导致子宫内膜癌细胞(ECCs)对激素治疗不敏感,甚至对放疗和放化疗产生抗性。因此,GLUT抑制剂有望成为EC精准靶向治疗的增敏剂。本综述旨在总结ECCs中GLUTs的表达调控、功能及治疗敏感性,旨在为EC的更好诊断和治疗提供新线索。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b4a0/9389465/c10719c978f2/fonc-12-933827-g001.jpg

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