Yoshida Go J
Department of Pathological Cell Biology, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan.
Japan Society for the Promotion of Science, 5-3-1 Kojimachi, Chiyoda-ku, Tokyo, 102-0083, Japan.
J Hematol Oncol. 2017 Mar 9;10(1):67. doi: 10.1186/s13045-017-0436-9.
The 2016 Nobel Prize in Physiology or Medicine was awarded to the researcher that discovered autophagy, which is an evolutionally conserved catabolic process which degrades cytoplasmic constituents and organelles in the lysosome. Autophagy plays a crucial role in both normal tissue homeostasis and tumor development and is necessary for cancer cells to adapt efficiently to an unfavorable tumor microenvironment characterized by hypo-nutrient conditions. This protein degradation process leads to amino acid recycling, which provides sufficient amino acid substrates for cellular survival and proliferation. Autophagy is constitutively activated in cancer cells due to the deregulation of PI3K/Akt/mTOR signaling pathway, which enables them to adapt to hypo-nutrient microenvironment and exhibit the robust proliferation at the pre-metastatic niche. That is why just the activation of autophagy with mTOR inhibitor often fails in vain. In contrast, disturbance of autophagy-lysosome flux leads to endoplasmic reticulum (ER) stress and an unfolded protein response (UPR), which finally leads to increased apoptotic cell death in the tumor tissue. Accumulating evidence suggests that autophagy has a close relationship with programmed cell death, while uncontrolled autophagy itself often induces autophagic cell death in tumor cells. Autophagic cell death was originally defined as cell death accompanied by large-scale autophagic vacuolization of the cytoplasm. However, autophagy is a "double-edged sword" for cancer cells as it can either promote or suppress the survival and proliferation in the tumor microenvironment. Furthermore, several studies of drug re-positioning suggest that "conventional" agents used to treat diseases other than cancer can have antitumor therapeutic effects by activating/suppressing autophagy. Because of ever increasing failure rates and high cost associated with anticancer drug development, this therapeutic development strategy has attracted increasing attention because the safety profiles of these medicines are well known. Antimalarial agents such as artemisinin and disease-modifying antirheumatic drug (DMARD) are the typical examples of drug re-positioning which affect the autophagy regulation for the therapeutic use. This review article focuses on recent advances in some of the novel therapeutic strategies that target autophagy with a view to treating/preventing malignant neoplasms.
2016年诺贝尔生理学或医学奖授予了发现自噬的研究人员。自噬是一种进化上保守的分解代谢过程,可在溶酶体中降解细胞质成分和细胞器。自噬在正常组织稳态和肿瘤发展中都起着关键作用,是癌细胞有效适应以低营养条件为特征的不利肿瘤微环境所必需的。这种蛋白质降解过程导致氨基酸循环利用,为细胞存活和增殖提供了足够的氨基酸底物。由于PI3K/Akt/mTOR信号通路失调,自噬在癌细胞中被组成性激活,这使它们能够适应低营养微环境,并在转移前生态位表现出强劲的增殖。这就是为什么仅用mTOR抑制剂激活自噬往往徒劳无功的原因。相反,自噬-溶酶体通量的紊乱会导致内质网(ER)应激和未折叠蛋白反应(UPR),最终导致肿瘤组织中凋亡细胞死亡增加。越来越多的证据表明,自噬与程序性细胞死亡密切相关,而不受控制的自噬本身往往会在肿瘤细胞中诱导自噬性细胞死亡。自噬性细胞死亡最初被定义为伴有细胞质大规模自噬空泡化的细胞死亡。然而,自噬对癌细胞来说是一把“双刃剑”,因为它既可以促进也可以抑制肿瘤微环境中的存活和增殖。此外,几项药物重新定位研究表明用于治疗非癌症疾病的“传统”药物可以通过激活/抑制自噬产生抗肿瘤治疗效果。由于抗癌药物开发的失败率不断上升且成本高昂,这种治疗开发策略越来越受到关注,因为这些药物的安全性已为人所知。青蒿素等抗疟药物和改善病情抗风湿药(DMARD)是药物重新定位的典型例子,它们通过影响自噬调节用于治疗。这篇综述文章重点关注了一些以自噬为靶点治疗/预防恶性肿瘤的新型治疗策略的最新进展。