揭示 p53 介导的肿瘤抑制机制。
Unravelling mechanisms of p53-mediated tumour suppression.
机构信息
Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, CCSR-South, Room 1255, 269 Campus Drive, Stanford, California 94305, USA.
1] Division of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, CCSR-South, Room 1255, 269 Campus Drive, Stanford, California 94305, USA. [2] Department of Genetics, Stanford University School of Medicine, CCSR-South, Room 1255, 269 Campus Drive, Stanford, California 94305, USA.
出版信息
Nat Rev Cancer. 2014 May;14(5):359-70. doi: 10.1038/nrc3711. Epub 2014 Apr 17.
p53 is a crucial tumour suppressor that responds to diverse stress signals by orchestrating specific cellular responses, including transient cell cycle arrest, cellular senescence and apoptosis, which are all processes associated with tumour suppression. However, recent studies have challenged the relative importance of these canonical cellular responses for p53-mediated tumour suppression and have highlighted roles for p53 in modulating other cellular processes, including metabolism, stem cell maintenance, invasion and metastasis, as well as communication within the tumour microenvironment. In this Opinion article, we discuss the roles of classical p53 functions, as well as emerging p53-regulated processes, in tumour suppression.
p53 是一种关键的肿瘤抑制因子，它通过协调特定的细胞反应来响应多种应激信号，包括短暂的细胞周期停滞、细胞衰老和细胞凋亡，这些都是与肿瘤抑制相关的过程。然而，最近的研究挑战了这些经典的细胞反应对于 p53 介导的肿瘤抑制的相对重要性，并强调了 p53 在调节其他细胞过程中的作用，包括代谢、干细胞维持、侵袭和转移，以及肿瘤微环境中的细胞间通讯。在这篇观点文章中，我们讨论了经典的 p53 功能以及新兴的 p53 调节过程在肿瘤抑制中的作用。
Zotero 插件