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RARbeta2 specificity in mediating RA inhibition of growth of lung cancer-derived cells

A Toulouse1, J Morin, P A Dion

  • 1Centre de Recherche du CHUM, Pavillon Notre-Dame, 1560 Sherbrooke E., Montréal, Canada. mbem@musica.mcgill.ca

Lung Cancer (Amsterdam, Netherlands)
|March 16, 2000
PubMed

Insights

Retinoic acid receptor beta 2 (RARbeta2) specifically suppresses lung cancer cell growth. Other retinoic acid receptor isoforms, like RARalpha1 and RARbeta1, do not exhibit this same tumor-suppressive effect.

Area of Science:

  • Molecular Biology
  • Oncology
  • Cell Biology

Background:

  • Retinoic acid receptor beta (RARbeta) is linked to growth suppression in epithelial tumors.
  • RARbeta2 has previously shown potential in reducing lung tumor cell growth and tumorigenicity.
  • The isoform specificity of this growth suppressive effect remained unclear.

Purpose of the Study:

  • To investigate the isoform specificity of retinoic acid receptor (RAR)-mediated growth suppression in lung cancer.
  • To determine if RARalpha1, RARbeta1, or RARbeta2 isoforms mediate the growth suppressive effects of retinoic acid.

Main Methods:

  • Transfection of RARalpha1, RARbeta1, and RARbeta2 into the Calu-1 epidermoid lung cancer cell line.
  • Assessment of in vitro growth capacities of transfected lung cancer cells.
  • Analysis of RARalpha2 expression patterns in various tumor-derived cell lines.

Main Results:

  • RARbeta2 transfection significantly reduced in vitro growth of Calu-1 cells in the presence of retinoic acid.
  • Expression of RARbeta1 or RARalpha1 isoforms did not replicate the growth suppressive effect of RARbeta2.
  • RARalpha2 expression patterns suggest it is not involved in retinoic acid-mediated growth suppression of lung cancer.

Conclusions:

  • The growth suppressive effect of retinoic acid in lung cancer is RARbeta2 isoform specific.
  • RARbeta1 and RARalpha1 isoforms do not mediate the observed tumor suppressive effects.
  • RARbeta2 represents a specific therapeutic target for retinoic acid-driven lung cancer growth inhibition.

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