Role of autophagy in acute myeloid leukemia therapy  

作　　者：Su-Ping Zhang Yu-Na Niu Na Yuan Ai-Hong Zhang Dan Chao Qiu-Ping Xu Li-Jun Wang Xue-Guang Zhang Wen-Li Zhao Yun Zhao Jian-Rong Wang 

机构地区：[1]The Cyrus Tang Hematology Center [2]The Cyrus Tang Hematology Center,Suzhou, Jiangsu 215123, P. R. China [3]Jiangsu Key Laboratory for Stem Cell Research,Suzhou, Jiangsu 215123, P. R. China [4]Children's Hospital, Soochow University,Suzhou, Jiangsu 215123, P. R. China

出　　处：《Chinese Journal of Cancer》2013年第3期130-135,共6页

基　　金：supported by grants from National Science Foundation of China (No. 31071258);The Ministry of Science and Technology of China (Pre-973 Plan: No. 2011CB512101; 863 Plan: No. 2011AA020114);a project funded by the Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)

摘　　要：Despite its dual role in determining cell fate in a wide array of solid cancer cell lines, autophagy has been robustly shown to suppress or kill acute myeloid leukemia cells via degradation of the oncogenic fusion protein that drives leukemogenesis. However, autophagy also induces the demise of acute leukemia cells that do not express the known fusion protein, though the molecular mechanism remains elusive. Nevertheless, since it can induce cooperation with apoptosis and differentiation in response to autophagic signals, autophagy can be manipulated for a better therapy on acute myeloid leukemia.Despite its dual role in determining cell fate in a wide array of solid cancer cell lines, autophagy has been robustly shown to suppress or kill acute myeloid leukemia cells via degradation of the oncogenic fusion protein that drives leukemogenesis. However, autophagy also induces the demise of acute leukemia cells that do not express the known fusion protein, though the molecular mechanism remains elusive. Nevertheless, since it can induce cooperation with apoptosis and differentiation in response to autophagic signals, autophagy can be manipulated for a better therapy on acute myeloid leukemia.

关 键 词：白血病细胞 髓细胞 自噬 急性 治疗 融合蛋白 肿瘤细胞株 分子机制 

分 类 号：R733.71[医药卫生—肿瘤]