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二酰甘油酰基转移酶1(DGAT1)可保护肿瘤免受脂毒性影响,成为一种很有前景的癌症治疗代谢靶点。

DGAT1 protects tumor from lipotoxicity, emerging as a promising metabolic target for cancer therapy.

作者信息

Cheng Xiang, Geng Feng, Guo Deliang

机构信息

Department of Radiation Oncology, James Comprehensive Cancer Center and College of Medicine at the Ohio State University, Columbus, OH, USA.

Center for Cancer Metabolism, James Comprehensive Cancer Center at the Ohio State University, Columbus, OH, USA.

出版信息

Mol Cell Oncol. 2020 Sep 8;7(6):1805257. doi: 10.1080/23723556.2020.1805257.

Abstract

We recently demonstrated that glioblastoma, the most lethal brain cancer, upregulates diacylglycerol O-acyltransferase 1 (DGAT1) to store excess fatty acids into triglycerides to prevent lipotoxicity and promote tumor growth. Targeting DGAT1 resulted in marked tumor cell death by triggering extensive oxidative stress, indicating that DGAT1 could be a promising target for cancer therapy.

摘要

我们最近证明,最致命的脑癌——胶质母细胞瘤,会上调二酰甘油O-酰基转移酶1(DGAT1),将多余的脂肪酸储存为甘油三酯,以防止脂毒性并促进肿瘤生长。靶向DGAT1通过引发广泛的氧化应激导致显著的肿瘤细胞死亡,这表明DGAT1可能是癌症治疗的一个有前景的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/acca/7671038/7cfacdf273cd/KMCO_A_1805257_F0001_OC.jpg

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