FHL2 interacts with iASPP and impacts the biological functions of leukemia cells
Metrics: PDF 1143 views | HTML 1677 views | ?
Wenting Lu1, Tengteng Yu1, Shuang Liu1, Saisai Li1, Shouyun Li1, Jia Liu1, Yingxi Xu1, Haiyan Xing1, Zheng Tian1, Kejing Tang1, Qing Rao1, Jianxiang Wang1 and Min Wang1
1State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin 300020, China
Jianxiang Wang, email: firstname.lastname@example.org
Min Wang, email: email@example.com
Keywords: FHL2, iASPP, biological functions, leukemia
Received: December 23, 2016 Accepted: March 09, 2017 Published: March 28, 2017
iASPP is an inhibitory member of apoptosis-stimulating proteins of p53 (ASPP) family, which inhibits p53-dependent apoptosis. iASPP was highly expressed in acute leukemia, inhibited leukemia cells apoptosis and promoted leukemogenesis. In order to clarify its mechanism, a yeast two-hybrid screen was performed and FHL2 was identified for the first time as one of the binding proteins of iASPP. FHL2 was highly expressed in K562 and Kasumi-1 cells. FHL2 and iASPP interacted with each other and co-localized in both nucleus and cytoplasm. Either FHL2 or iASPP silenced could reduce cell proliferation, induce cell cycle arrest at G0/G1 phase, and increase cell apoptosis. Western blot analysis showed that the level of p21 and p27 increased, CDK4, E2F1, Cyclin E and anti-apoptotic proteins Bcl-2 and Bcl-xL reduced. Interestingly, when FHL2 was knocked down, the protein expression level of iASPP also decreased. Similarly, the expression of FHL2 would reduce when iASPP was silenced. These results indicated that FHL2 might be a novel potential target for acute myelocytic leukemia treatment.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.