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Acetylcholinesterase is associated with a decrease in cell proliferation of hepatocellular carcinoma cells.

Authors :
Pérez-Aguilar B
Vidal CJ
Palomec G
García-Dolores F
Gutiérrez-Ruiz MC
Bucio L
Gómez-Olivares JL
Gómez-Quiroz LE
Source :
Biochimica et biophysica acta [Biochim Biophys Acta] 2015 Jul; Vol. 1852 (7), pp. 1380-7. Date of Electronic Publication: 2015 Apr 11.
Publication Year :
2015

Abstract

Acetylcholinesterase (AChE), the enzyme that rapidly splits acetylcholine into acetate and choline, presents non-cholinergic functions through which may participate in the control of cell proliferation and apoptosis. These two features are relevant in cancer, particularly in hepatocellular carcinoma (HCC), a very aggressive liver tumor with high incidence and poor prognosis in advanced stages. Here we explored the relation between acetylcholinesterase and HCC growth by testing the influence of AChE on proliferation of Huh-7 and HepG2 cell lines, addressed in monolayer cultures, spheroid formation and human liver tumor samples. Results showed a clear relation in AChE expression and cell cycle progression, an effect which depended on cell confluence. Inhibition of AChE activity led to an increase in cell proliferation, which was associated with downregulation of p27 and cyclins. The fact that Huh-7 and HepG2 cell lines provided similar results lent weight to the relationship of AChE expression with cell cycle progression in hepatoma cell lines at least. Human liver tumor samples exhibited a decrease in AChE activity as compared with normal tissue. The evidence presented herein provides additional support for the proposed tumor suppressor role of AChE, which makes it a potential therapeutic target in therapies against hepatocellular carcinoma.<br /> (Copyright © 2015 Elsevier B.V. All rights reserved.)

Details

Language :
English
ISSN :
0006-3002
Volume :
1852
Issue :
7
Database :
MEDLINE
Journal :
Biochimica et biophysica acta
Publication Type :
Academic Journal
Accession number :
25869328
Full Text :
https://doi.org/10.1016/j.bbadis.2015.04.003