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Enhancement of gap junctional intercellular communication by dibutyryl cyclic AMP in lung epithelial cells
R W Banoub1, M Fernstrom, A M Malkinson
1Department of Pathology, Medical College of Ohio, Toledo 43699, USA.
Abstract:
Reduced gap junctional intercellular communication (GJIC) occurs in neoplastic cells and contributes to their phenotype. Cyclic AMP agonists inhibit lung cancer cell growth and enhance GIIC in other cell types, but little is known about their effects on lung epithelial cell gap junctions. We have examined whether N6, 2'-O-dibutyryladenosine 3':5'-cyclic mono-phosphate (DBcAMP) affected GJIC, gap junction protein (connexin43) expression, and the growth of non-transformed and neoplastic mouse lung epithelial cells. DBcAMP (0.01.1 mM) stimulated GJIC (assayed by fluorescent dye microinjection) and connexin43 expression (assessed by Northern and Western blotting) and reduced their proliferation. These results suggest an association between cAMP growth inhibition and enhanced GJIC in lung epithelial cells.
Insights
Cyclic adenosine monophosphate (cAMP) agonists like DBcAMP enhance gap junctional intercellular communication (GJIC) and connexin43 expression in lung epithelial cells. This suggests a link between cAMP-mediated growth inhibition and improved GJIC in lung cancer research.
Area of Science:
- Cell Biology
- Molecular Biology
- Cancer Research
Background:
- Reduced gap junctional intercellular communication (GJIC) is a hallmark of neoplastic cells, contributing to their aberrant phenotype.
- Cyclic adenosine monophosphate (cAMP) agonists are known to inhibit cancer cell growth and enhance GJIC in various cell types, but their specific effects on lung epithelial cells remain largely unexplored.
Purpose of the Study:
- To investigate the impact of N6, 2'-O-dibutyryladenosine 3':5'-cyclic mono-phosphate (DBcAMP), a cAMP agonist, on GJIC, connexin43 expression, and proliferation in both non-transformed and neoplastic mouse lung epithelial cells.
Main Methods:
- Utilized fluorescent dye microinjection to assay GJIC.
- Employed Northern and Western blotting techniques to assess connexin43 protein and mRNA expression.
- Measured cell proliferation rates in response to DBcAMP treatment.
Main Results:
- DBcAMP treatment significantly stimulated GJIC in lung epithelial cells.
- Connexin43 expression, at both protein and mRNA levels, was upregulated by DBcAMP.
- DBcAMP effectively reduced the proliferation of both non-transformed and neoplastic lung epithelial cells.
Conclusions:
- The study demonstrates a positive correlation between cAMP-mediated growth inhibition and enhanced GJIC in lung epithelial cells.
- Findings suggest that targeting cAMP pathways could be a viable strategy for modulating GJIC and inhibiting lung cancer cell growth.