AKT and the Hallmarks of Cancer

癌症 PI3K/AKT/mTOR通路 癌变 受体酪氨酸激酶 表观遗传学 重编程 癌症研究 细胞信号 肿瘤微环境 蛋白激酶B 激酶 神经科学 生物 细胞 遗传学 细胞生物学 信号转导 基因
作者
Eleonora Sementino,Dalal Hassan,Alfonso Bellacosa,Joseph R. Testa
出处
期刊:Cancer Research [American Association for Cancer Research]
卷期号:84 (24): 4126-4139 被引量:16
标识
DOI:10.1158/0008-5472.can-24-1846
摘要

Abstract Nearly a quarter century ago, Hanahan and Weinberg conceived six unifying principles explaining how normal cells transform into malignant tumors. Their provisional set of biological capabilities acquired during tumor development—cancer hallmarks—would evolve to 14 tenets as knowledge of cancer genomes, molecular mechanisms, and the tumor microenvironment expanded, most recently adding four emerging enabling characteristics: phenotypic plasticity, epigenetic reprogramming, polymorphic microbiomes, and senescent cells. AKT kinases are critical signaling molecules that regulate cellular physiology upon receptor tyrosine kinases and PI3K activation. The complex branching of the AKT signaling network involves several critical downstream nodes that significantly magnify its functional impact, such that nearly every organ system and cell in the body may be affected by AKT activity. Conversely, tumor-intrinsic dysregulation of AKT can have numerous adverse cellular and pathologic ramifications, particularly in oncogenesis, as multiple tumor suppressors and oncogenic proteins regulate AKT signaling. Herein, we review the mounting evidence implicating the AKT pathway in the aggregate of currently recognized hallmarks of cancer underlying the complexities of human malignant diseases. The challenges, recent successes, and likely areas for exciting future advances in targeting this complex pathway are also discussed.
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