ADCY7 supports development of acute myeloid leukemia

作者:Li, Chunling; Xie, Jingjing; Lu, Zhigang; Chen, Chen; Yin, Yancun; Zhan, Renhui; Fang, Yi; Hu, Xuemei; Zhang, Cheng Cheng*
来源:Biochemical and Biophysical Research Communications, 2015, 465(1): 47-52.
DOI:10.1016/j.bbrc.2015.07.123

摘要

Acute myeloid leukemia (AML) is the most common adult acute leukemia. Despite treatment, the majority of the AML patients relapse within 5 years. In silico analysis of several available databases of AML patients showed that the expression of adenylate cyclase 7 (ADCY7) significantly inversely correlates with the overall survival of AML patients. To determine whether ADCY7 supports AML development, we employed an shRNA-encoding lentivirus system to inhibit adcy7 expression in human AML cells including U937, MV4-11, and THP-1 cells. The ADCY7 deficiency resulted in decreased cell growth, elevated apoptosis, and lower c-Myc expression of these leukemia cells. This indicates that G protein-coupled receptor signaling contributes to AML pathogenesis. Our study suggests that inhibition of ADCY7 may be novel strategy for treating leukemia.