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ADCY7 supports development of acute myeloid leukemia.

ABSTRACT: 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.

SUBMITTER: Li C

PROVIDER: S-EPMC4554980 | biostudies-literature | 2015 Sep

REPOSITORIES: biostudies-literature

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ADCY7 supports development of acute myeloid leukemia.

Li Chunling C Xie Jingjing J Lu Zhigang Z Chen Chen C Yin Yancun Y Zhan Renhui R Fang Yi Y Hu Xuemei X Zhang Cheng Cheng CC

Biochemical and biophysical research communications 20150726 1

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 incl ...[more]

PMID: 26220344

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