作者: Wenting Lu , Tengteng Yu , Shuang Liu , Saisai Li , Shouyun Li
DOI: 10.18632/ONCOTARGET.16617
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摘要: // Wenting Lu 1 , Tengteng Yu Shuang Liu Saisai Li Shouyun Jia Yingxi Xu Haiyan Xing Zheng Tian Kejing Tang Qing Rao Jianxiang Wang and Min State Key Laboratory of Experimental Hematology, Institute Hematology Blood Diseases Hospital, Chinese Academy Medical Sciences & Peking Union College, Tianjin 300020, China Correspondence to: Wang, email: wangjx@ihcams.ac.cn wangjxm@ihcams.ac.cn Keywords: FHL2, iASPP, biological functions, leukemia Received: December 23, 2016 Accepted: March 09, 2017 Published: 28, 2017 ABSTRACT iASPP is an inhibitory member apoptosis-stimulating proteins p53 (ASPP) family, which inhibits p53-dependent apoptosis. was highly expressed in acute leukemia, inhibited cells apoptosis promoted leukemogenesis. In order to clarify its mechanism, a yeast two-hybrid screen performed FHL2 identified for the first time as one binding iASPP. K562 Kasumi-1 cells. interacted with each other co-localized both nucleus cytoplasm. Either or silenced could reduce cell proliferation, induce cycle arrest at G0/G1 phase, increase Western blot analysis showed that level p21 p27 increased, CDK4, E2F1, Cyclin E anti-apoptotic Bcl-2 Bcl-xL reduced. Interestingly, when knocked down, protein expression also decreased. Similarly, would silenced. These results indicated might be novel potential target myelocytic treatment.