Literature DB >> 26220344

ADCY7 supports development of acute myeloid leukemia.

Chunling Li1, Jingjing Xie2, Zhigang Lu3, Chen Chen1, Yancun Yin1, Renhui Zhan1, Yi Fang3, Xuemei Hu1, Cheng Cheng Zhang4.   

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.
Copyright © 2015 Elsevier Inc. All rights reserved.

Entities:  

Keywords:  ADCY7; Acute myeloid leukemia; Apoptosis; Cell growth; G protein-coupled receptor; shRNA

Mesh:

Substances:

Year:  2015        PMID: 26220344      PMCID: PMC4554980          DOI: 10.1016/j.bbrc.2015.07.123

Source DB:  PubMed          Journal:  Biochem Biophys Res Commun        ISSN: 0006-291X            Impact factor:   3.575


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