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Bcl-2 gene prevents apoptosis in murine acth-secreting adenoma cells induced by bromocriptine

D Yin1, S Kondo, J Takeuchi

  • 1NATL UTANO HOSP,DEPT NEUROSURG,8 ONDOYAMA CHO,UKYO KU,KYOTO 616,JAPAN. STANFORD UNIV,DEPT PATHOL,STANFORD,CA 94305.

International Journal of Oncology
|May 14, 2011
PubMed

Insights

Bromocriptine induces apoptosis in pituitary adenoma cells. Overexpressing the bcl-2 gene in these cells, however, confers resistance to bromocriptine-induced cell death, suggesting bcl-2

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Oncology

Background:

  • Bromocriptine is a primary treatment for pituitary adenomas.
  • The precise mechanism of bromocriptine's tumor-shrinking effect is unclear.
  • Apoptosis induction by bromocriptine was recently observed in pituitary tumor cells.

Purpose of the Study:

  • To investigate the role of the bcl-2 gene in bromocriptine-induced apoptosis.
  • To determine if bcl-2 overexpression affects bromocriptine's efficacy in pituitary adenoma cells.

Main Methods:

  • Murine ACTH-secreting pituitary adenoma (AtT-20) cells were used.
  • Retroviral gene transfer was employed to enforce bcl-2 gene expression.
  • Cells with and without bcl-2 overexpression were treated with bromocriptine.
  • Apoptosis was assessed to evaluate treatment effects.

Main Results:

  • Bromocriptine treatment induced apoptosis in AtT-20 cells.
  • Enforced expression of the bcl-2 gene significantly increased resistance to bromocriptine-induced apoptosis.
  • This suggests bcl-2 plays a role in mediating sensitivity to bromocriptine.

Conclusions:

  • The bcl-2 gene is implicated in the apoptotic response to bromocriptine in pituitary adenoma cells.
  • Upregulation of bcl-2 can confer resistance to bromocriptine therapy.
  • Targeting bcl-2 pathways may offer strategies to overcome treatment resistance in pituitary adenomas.

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