ADCY7 supports development of acute myeloid leukemia.

Biochem Biophys Res Commun

Department of Physiology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA; Department of Developmental Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Electronic address:

Published: September 2015

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.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4554980PMC
http://dx.doi.org/10.1016/j.bbrc.2015.07.123DOI Listing

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