p53, autophagy and tumor suppression
p53, autophagy and tumor suppression
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DOI：
10.4161/auto.1.3.2051
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发表时间：
2005-10-01
期刊：
影响因子：
13.3
通讯作者：
Jin, SK
中科院分区：
文献类型：
--
作者：
Jin, SK
自噬最近被确立为一种新的肿瘤抑制机制，这刺激了一波旨在确切了解自噬如何防止肿瘤发生的研究，以及确定自噬在人类癌症中的影响程度。自噬可能在亚细胞水平上通过清除有缺陷的细胞质成分（如受损的线粒体）发挥其肿瘤抑制功能。此外，它可能在细胞水平上发挥作用，帮助有序地清除受损细胞。先前的研究表明，自噬在人类乳腺癌、卵巢癌和前列腺癌中受到损害。最近的研究表明，自噬是由p53激活的，p53是一种关键的肿瘤抑制因子，参与了大多数（如果不是全部）肿瘤的发生。这项研究将自噬置于人类癌症的更广泛背景下。未来的工作阐明了自噬在p53电路和p53功能中的作用，可能会为肿瘤发生和靶向癌症化疗提供更多的见解。
Autophagy was recently established as a novel tumor suppression mechanism, which stimulated a wave of investigations that were aimed at understanding exactly how autophagy prevents tumorigenesis, as well as to determine to what extent autophogy is implicated in human cancers. Autophagy might exert its tumor suppression function at the subcellular level by removing defective cytoplasmic components, such as damaged mitochondria. In addition, it might function at the cellular level by helping in the orderly removal of damaged cells. Previous studies indicated that autophagy is compromised in human breast, ovarian and prostate cancers. Recent research revealed that autophogy is activated by p53, a critical tumor suppressor that is involved in most, if not all, tumorigenesis. This study places autophagy in a broader context of human cancers. Future work elucidating the role of autophagy in the p53 circuit and p53 function might provide more insight into tumorigenesis and targeted cancer chemotherapy.