Department of Medical Oncology, Inselspital, Bern University Hospital, Bern, Switzerland.
J Intern Med. 2010 Nov;268(5):410-8. doi: 10.1111/j.1365-2796.2010.02266.x.
Autophagy (literally self-eating) is a catabolic mechanism involved in the recycling and turnover of cytoplasmic constituents. Although often referred to as type II programmed cell death, autophagy is primarily a survival rather than a cell death mechanism in response to different stress stimuli. Autophagy is a process in which part of the cytoplasm or entire organelles are sequestered into double-membrane vesicles, called autophagosomes, which ultimately fuse with lysosomes to degrade their contents. Studies show that autophagy is associated with a number of pathological conditions, including cancer, infectious diseases, myopathies and neurodegenerative disorders. With respect to cancer, it has been suggested that the early stages of tumourigenesis are associated with downregulation of autophagy-related (ATG) genes. Indeed, several ATG genes display tumour suppressor function, including Beclin1, which is frequently hemizygously deleted in breast cancer cells. Conversely, in advanced stages of tumourigenesis or during anticancer therapy, autophagy may promote survival of tumour cells in adverse environmental conditions. Therefore, a thorough understanding of autophagy in different cancer types and stages is a prerequisite to determine an autophagy-activating or autophagy-inhibiting treatment strategy.
自噬（字面意思是“自我吞噬”）是一种参与细胞质成分回收和周转的分解代谢机制。尽管自噬通常被称为 2 型程序性细胞死亡，但它主要是一种生存机制，而不是对不同应激刺激的细胞死亡机制。自噬是一种将部分细胞质或整个细胞器隔离到双层膜囊泡（称为自噬体）中的过程，自噬体最终与溶酶体融合以降解其内容物。研究表明，自噬与许多病理状况有关，包括癌症、传染病、肌肉疾病和神经退行性疾病。就癌症而言，已经表明肿瘤发生的早期阶段与自噬相关（ATG）基因的下调有关。事实上，一些 ATG 基因具有肿瘤抑制功能，包括 Beclin1，其在乳腺癌细胞中经常呈半合子缺失。相反，在肿瘤发生的晚期或在抗癌治疗期间，自噬可能促进肿瘤细胞在不利环境条件下的存活。因此，深入了解不同类型和阶段的癌症中的自噬是确定自噬激活或自噬抑制治疗策略的前提。
