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Isolation of Lung Retinoid-Containing Cells by Cell Sorting
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Cyclic adenosine monophosphate-dependent cell type-specific modulation of mitogenic signaling by retinoids in normal

Hussein A N Al-Wadei1, Hildegard M Schuller

  • 1Experimental Oncology Laboratory, Department of Pathobiology, College of Veterinary Medicine, University of Tennessee, Knoxville, TN 37996, USA.

Cancer Detection and Prevention
|October 28, 2006
PubMed
Abstract

Insights

Retinoids 9-cis-retinoic acid (9-Cis-RA) and 13-cis-retinoic acid (13-Cis-RA) activate cAMP and PKA. This may inhibit small cell lung cancer but promote adenocarcinoma.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Lung cancer is a leading cause of cancer death globally.
  • Fruit and vegetable consumption may reduce lung cancer risk.
  • Previous trials with beta-carotene and retinoids showed increased mortality.

Purpose of the Study:

  • Investigate the effects of 9-cis-retinoic acid (9-Cis-RA) and 13-cis-retinoic acid (13-Cis-RA) on lung cancer cells.
  • Examine the role of cAMP, PKA, and ERK1/2 pathways in retinoid-induced effects.

Main Methods:

  • Utilized MTT assays for cell proliferation.
  • Employed cAMP immunoassays and PKA activation assays.
  • Analyzed ERK1/2 phosphorylation using Western blots in various human lung cell lines.

Main Results:

  • Both 9-Cis-RA and 13-Cis-RA increased intracellular cAMP and PKA activation in all tested cell lines.
  • In BEAS-2B and NCI-H69 cells, cAMP/PKA stimulation reduced ERK1/2 phosphorylation and inhibited cell proliferation.
  • Conversely, in HPL1D and NCI-H322 cells, cAMP/PKA stimulation increased ERK1/2 phosphorylation and cell proliferation.

Conclusions:

  • Identified a novel mechanism: 9-Cis-RA and 13-Cis-RA activate PKA via increased cAMP.
  • cAMP/PKA stimulation may inhibit small cell lung carcinoma and large airway epithelial tumors.
  • This pathway may selectively promote lung adenocarcinoma development from small airway epithelial cells.

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