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ADCY7 supports development of acute myeloid leukemia.
- Source :
-
Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2015 Sep 11; Vol. 465 (1), pp. 47-52. Date of Electronic Publication: 2015 Jul 26. - Publication Year :
- 2015
-
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.<br /> (Copyright © 2015 Elsevier Inc. All rights reserved.)
- Subjects :
- Adenylyl Cyclases metabolism
Apoptosis genetics
Cell Cycle genetics
Cell Line, Tumor
Cell Proliferation
Cytoskeletal Proteins genetics
Cytoskeletal Proteins metabolism
Genetic Vectors
Humans
Lentivirus genetics
Leukemia, Myeloid, Acute classification
Leukemia, Myeloid, Acute mortality
Leukemia, Myeloid, Acute pathology
Proto-Oncogene Proteins c-myc antagonists & inhibitors
Proto-Oncogene Proteins c-myc metabolism
RNA, Small Interfering genetics
RNA, Small Interfering metabolism
Receptors, G-Protein-Coupled genetics
Receptors, G-Protein-Coupled metabolism
Signal Transduction
Survival Analysis
Adenylyl Cyclases genetics
Gene Expression Regulation, Leukemic
Leukemia, Myeloid, Acute genetics
Proto-Oncogene Proteins c-myc genetics
Subjects
Details
- Language :
- English
- ISSN :
- 1090-2104
- Volume :
- 465
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Biochemical and biophysical research communications
- Publication Type :
- Academic Journal
- Accession number :
- 26220344
- Full Text :
- https://doi.org/10.1016/j.bbrc.2015.07.123