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[Bcl-2 tumor suppressor as a possible mediator between genotoxic stress and disturbance in hormonal homeostasis]

S Iu Revskoĭ1

  • 1N.N. Petrov Research Institute of Oncology, Ministry of Health of the RF, St. Petersburg, Russia.

Voprosy Onkologii
|June 1, 2001
PubMed

Insights

The tumor suppressor gene bcl-2 enhances resistance to glucocorticoids by preventing apoptosis. Overexpression of bcl-2 disrupts the negative feedback regulation of proopiomelanocortin (POMC) and ACTH secretion.

Area of Science:

  • Molecular Biology
  • Endocrinology
  • Cell Biology

Background:

  • The tumor suppressor gene bcl-2 is implicated in cellular resistance to apoptosis induced by various factors, including glucocorticoids.
  • Glucocorticoids play a crucial role in regulating hormonal homeostasis through negative feedback mechanisms.

Purpose of the Study:

  • To investigate the role of bcl-2 in the negative feedback regulation mediated by glucocorticoids.
  • To determine if bcl-2 influences glucocorticoid-induced suppression of proopiomelanocortin (POMC) gene expression and ACTH secretion.

Main Methods:

  • Transient transfection of the bcl-2 gene into murine corticotrope AtT-20 cells.
  • Treatment of transfected cells with varying concentrations of dexamethasone.
  • Measurement of proopiomelanocortin (POMC) gene expression and ACTH secretion.

Main Results:

  • Overexpression of bcl-2 conferred significant resistance to dexamethasone-induced down-regulation of POMC gene expression and ACTH secretion.
  • Bcl-2's activity was most pronounced at saturating dexamethasone concentrations (100 nM-1 mM).
  • Overexpression of bcl-2 interfered with receptor-mediated glucocorticoid activity, specifically affecting POMC/ACTH expression.

Conclusions:

  • Bcl-2 possesses a novel function as a regulator of hormonal homeostasis.
  • Bcl-2 may be involved in the hormonal and metabolic responses to genotoxic stress, potentially linking to carcinogenic aging.

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