肿瘤微环境
癌症研究
表观遗传学
自噬
癌症
癌细胞
细胞代谢
细胞生物学
细胞
生物
细胞凋亡
生物化学
遗传学
肿瘤细胞
基因
作者
Lulu Chen,Minglie Hu,Luojun Chen,Yangqin Peng,Zhen Cai,Xianding Wang,Xiangpan Li,Yi Yao,Qibin Song,J. Li,Huadong Pei
标识
DOI:10.1016/j.canlet.2024.216742
摘要
O-linked-N-acetylglucosaminylation (O-GlcNAcylation), a dynamic post-translational modification (PTM), holds profound implications in controlling various cellular processes such as cell signaling, metabolism, and epigenetic regulation that influence cancer progression and therapeutic resistance. From the therapeutic perspective, O-GlcNAc modulates drug efflux, targeting and metabolism. By integrating signals from glucose, lipid, amino acid, and nucleotide metabolic pathways, O-GlcNAc acts as a nutrient sensor and transmits signals to exerts its function on genome stability, epithelial-mesenchymal transition (EMT), cell stemness, cell apoptosis, autophagy, cell cycle. O-GlcNAc also attends to tumor microenvironment (TME) and the immune response. At present, several strategies aiming at targeting O-GlcNAcylation are under mostly preclinical evaluation, where the newly developed O-GlcNAcylation inhibitors markedly enhance therapeutic efficacy. Here we systematically outline the mechanisms through which O-GlcNAcylation influences therapy resistance and deliberate on the prospects and challenges associated with targeting O-GlcNAcylation in future cancer treatments.
科研通智能强力驱动
Strongly Powered by AbleSci AI