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自噬是一个细胞质成分被双层膜的囊泡包裹并与溶酶体融合降解的过程。肿瘤细胞利用自噬过程存活于代谢应激下,因此推测自噬抑制剂在肿瘤治疗中具有临床应用价值。与此相矛盾的是在人类乳腺肿瘤、卵巢肿瘤、前列腺肿瘤中,重要的自噬基因beclin1等位性丢失发生很频繁,表明自噬的受损促使肿瘤的发生。与自噬缺陷和对代谢应激损伤耐受有关的肿瘤,其发生的可能原因包括增加炎症反应导致的细胞死亡及细胞因子的产生,染色体组的损伤。这表明自噬诱导剂通过限制细胞基因组损伤、细胞死亡及炎症来预防肿瘤可能具有价值。因为自噬是细胞应激反应的重要组成部分,所以通过调节自噬过程进行肿瘤的预防及治疗将是一个很有前景的新领域。
Autophagy is a process in which cytoplasmic components are surrounded by vesicles of bilayer membranes and fuse with lysosomes. Tumor cells using autophagy survive in the metabolic stress, so speculated that autophagy inhibitors in the treatment of cancer has clinical value. Contrary to this, allelic loss of beclin1, an important autophagy gene, occurs frequently in human breast, ovarian, and prostate tumors, suggesting that autophagy impairs tumor development. Possible causes for autophagy defects and tumors associated with tolerance to metabolic stress injury include increased cell death and cytokine production as a result of inflammatory responses, and chromosomal damage. This suggests that it may be of value for an autophagy-inducing agent to prevent tumors by limiting cell genomic damage, cell death and inflammation. Because autophagy is an important part of cellular stress response, prevention and treatment of tumor by regulating autophagy will be a promising new field.