PI3K/AKT/mTOR通路
蛋白激酶B
癌变
生物
重编程
效应器
肿瘤微环境
细胞生物学
信号转导
机制(生物学)
代谢途径
细胞代谢
癌症研究
肿瘤进展
癌细胞
细胞信号
新陈代谢
癌症
细胞
肿瘤细胞
生物化学
遗传学
哲学
认识论
作者
Wen Su,Lü Tian,Lan Pin Guo,Lu Huang,Weiting Gao
标识
DOI:10.1016/j.bbcan.2023.188952
摘要
Oncogenic signaling involved in tumor metabolic reprogramming. Tumorigenesis was not only determined by the mutations or deletion of oncogenes but also accompanied by the reprogramming of cellular metabolism. Metabolic alterations play a crucial regulatory role in the development and progression of tumors. Oncogenic PI3K/AKT signaling mediates the metabolic switch in cancer cells and immune cells in the tumor microenvironment. PI3K/AKT and its downstream effector branch off and connect to multiple steps of metabolism, such as glucose, lipids, and amino acids. Thus, PI3K inhibitor could effectively regulate metabolic pathway and impede the oncogenic process and some key metabolic proteins or critical enzymes also constitute biomarkers for tumor diagnosis and treatment. In the current review, we summarize the significant effect of PI3K/AKT signaling toward tumor metabolism, it enables us to obtain the better understanding for this interaction and develop more effective therapeutic strategies targeting cancer cell metabolism.
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