p53 与肿瘤抑制：需要一个网络。
p53 and Tumor Suppression: It Takes a Network.
机构信息
Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Genetics, Stanford University School of Medicine, Stanford, CA 94305, USA; Stanford Cancer Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.
出版信息
Trends Cell Biol. 2021 Apr;31(4):298-310. doi: 10.1016/j.tcb.2020.12.011. Epub 2021 Jan 28.
The TP53 tumor suppressor is the most frequently mutated gene in human cancer. p53 suppresses tumorigenesis by transcriptionally regulating a network of target genes that play roles in various cellular processes. Though originally characterized as a critical regulator for responses to acute DNA damage (activation of apoptosis and cell cycle arrest), recent studies have highlighted new pathways and transcriptional targets downstream of p53 regulating genomic integrity, metabolism, redox biology, stemness, and non-cell autonomous signaling in tumor suppression. Here, we summarize our current understanding of p53-mediated tumor suppression, situating recent findings from mouse models and unbiased screens in the context of previous studies and arguing for the importance of the pleiotropic effects of the p53 transcriptional network in inhibiting cancer.
TP53 肿瘤抑制因子是人类癌症中最常发生突变的基因。p53 通过转录调控一系列在各种细胞过程中发挥作用的靶基因来抑制肿瘤发生。虽然最初被描述为对急性 DNA 损伤（激活细胞凋亡和细胞周期阻滞）反应的关键调节因子，但最近的研究强调了 p53 调节基因组完整性、代谢、氧化还原生物学、干细胞特性和肿瘤抑制中非细胞自主信号下游的新途径和转录靶标。在这里，我们总结了我们对 p53 介导的肿瘤抑制的现有认识，将来自小鼠模型和无偏筛选的最新发现置于以前研究的背景下，并认为 p53 转录网络的多效性效应对抑制癌症的重要性。
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