Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
Curr Opin Cell Biol. 2010 Apr;22(2):226-33. doi: 10.1016/j.ceb.2009.11.003. Epub 2009 Nov 28.
Autophagy, originally described as a universal lysosome-dependent bulk degradation of cytoplasmic components upon nutrient deprivation, has since been shown to influence diverse aspects of homeostasis and is implicated in a wide variety of pathological conditions, including cancer. The list of autophagy-related (Atg) genes associated with the initiation and progression of human cancer as well as with responses to cancer therapy continues to grow as these genes are being discovered. However, whether Atg genes work through their expected mechanisms of autophagy regulation and/or through as-yet-undefined functions in the development of cancer remains to be further clarified. Here we review recent advances in the knowledge of the molecular basis of autophagy genes and their biological outputs during tumor development. A better understanding of the mechanistic link between cellular autophagy and tumor growth control may ultimately better human cancer treatments.
自噬最初被描述为一种普遍的溶酶体依赖性的细胞质成分在营养缺乏时的批量降解，此后已被证明会影响内稳态的各个方面，并与多种病理状况有关，包括癌症。随着这些基因的发现，与人类癌症的发生和发展以及对癌症治疗的反应有关的自噬相关（Atg）基因的清单不断增加。然而，Atg 基因是否通过其预期的自噬调节机制以及通过在癌症发展中尚未定义的功能起作用，仍有待进一步澄清。在这里，我们回顾了自噬基因的分子基础及其在肿瘤发展过程中的生物学产物的最新进展。更好地理解细胞自噬与肿瘤生长控制之间的机制联系，最终可能会改善人类癌症的治疗方法。
