A quantitative inverse relationship between connexin32 expression and cell proliferation in a rat hepatoma cell line

Abstract Gap junctions comprised of connexin proteins are involved in direct intercellular communication and the regulation of cell behaviour and homeostasis. Reduced connexin expression and loss of gap junction function is a characteristic of many cancer cells and of the effect of many non-genotoxi...

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Bibliographic Details
Published in:Toxicology (Amsterdam) 2008-11, Vol.253 (1), p.46-52
Main Authors: Edwards, Gareth Owain, Jondhale, Shrikant, Chen, Tao, Chipman, J. Kevin
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Bromodeoxyuridine - metabolism
Carcinogenesis, carcinogens and anticarcinogens
Carcinoma, Hepatocellular - metabolism
Carcinoma, Hepatocellular - pathology
Cell Line, Tumor
Cell Proliferation
Chemical agents
Connexin32
Connexins - genetics
Connexins - metabolism
Dexamethasone - pharmacology
Emergency
G1 Phase
Gap junction
Gap Junction beta-1 Protein
Gastroenterology. Liver. Pancreas. Abdomen
Gene Expression Regulation, Neoplastic
Genes, cdc
Liver. Biliary tract. Portal circulation. Exocrine pancreas
Medical sciences
Non-genotoxic carcinogen
Polymerase Chain Reaction
Proliferation
Rats
RNA Interference
S Phase
Toxicology
Tubulin - metabolism
Tumors
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Summary:Abstract Gap junctions comprised of connexin proteins are involved in direct intercellular communication and the regulation of cell behaviour and homeostasis. Reduced connexin expression and loss of gap junction function is a characteristic of many cancer cells and of the effect of many non-genotoxic carcinogens that induce cell proliferation. Moreover, when certain cancer cell lines are transfected with specific connexin genes, cells can regain control over proliferation. We have employed RNA interference and dexamethasone to modulate connexin32 expression in MH1 C1 cells to a range of concentrations. This allowed the determination of the quantitative relationship between connexin32 protein expression and cell proliferation. The magnitude of cell proliferation, measured by bromodeoxyuridine incorporation, was inversely proportional to the level of connexin32 expression. Q-PCR indicated a lack of change of expression of a range of cell cycle-related genes at 24 h. The inverse relationship between Cx32 expression and proliferation was continuous, and a threshold level of reduction of connexin32 was not observable for an influence on proliferation.
ISSN:0300-483X
1879-3185
DOI:10.1016/j.tox.2008.08.010