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Related Experiment Videos

Altered glucocorticoid receptor expression and function during mouse skin carcinogenesis

I V Budunova1, S Carbajal, H Kang

  • 1Department of Carcinogenesis, University of Texas M. D. Anderson Cancer Center, Smithville 78957, USA.

Molecular Carcinogenesis
|March 1, 1997
PubMed
Summary

Glucocorticoid receptor (GR) expression and function are altered in mouse skin tumors. Early papillomas show decreased GR, while later tumors have normal or increased GR, yet lose sensitivity to glucocorticoids, suggesting a role in tumor promotion.

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Area of Science:

  • Dermatology
  • Oncology
  • Molecular Biology

Background:

  • Glucocorticoids inhibit skin tumor promotion but established papillomas resist this effect.
  • Glucocorticoid receptor (GR) mediates glucocorticoid actions.
  • Understanding GR in skin tumors is crucial for therapeutic strategies.

Purpose of the Study:

  • To investigate glucocorticoid receptor (GR) expression and function in mouse skin papillomas and squamous cell carcinomas.
  • To determine if GR alterations contribute to resistance to glucocorticoid-induced growth inhibition.

Main Methods:

  • SENCAR mice were subjected to a chemical carcinogenesis protocol to induce skin tumors.
  • Glucocorticoid receptor (GR) mRNA levels were assessed using Northern blotting.
  • GR binding assays and functional assays with fluocinolone acetonide (FA) were performed on normal epidermis, surrounding skin, and tumors.

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Main Results:

  • Early papillomas showed decreased GR mRNA and binding, while late papillomas and squamous cell carcinomas had normal or increased GR levels.
  • Fluocinolone acetonide (FA) inhibited keratinocyte proliferation and modulated gene expression in normal and hyperplastic skin but not in papillomas.
  • Glucocorticoid-responsive genes (metallothionein 1, connexin 26) were not affected by FA in tumors, indicating functional GR impairment.

Conclusions:

  • Alterations in both expression and function of the glucocorticoid receptor (GR) occur during skin tumor progression.
  • These GR changes may represent a key mechanism underlying tumor resistance to glucocorticoid-mediated growth inhibition.
  • Dysregulation of GR signaling contributes to skin tumor promotion and progression.