Induction of apoptosis in murine ACTH-secreting pituitary adenoma cells by bromocriptine

FEBS Lett. 1994 Feb 14;339(1-2):73-5. doi: 10.1016/0014-5793(94)80387-0.

Abstract

Bromocriptine, a dopamine agonist, is now an accepted primary therapeutic agent for patients with prolactinomas and other pituitary adenomas. In this study, we demonstrated that bromocriptine inhibited the proliferation of murine ACTH-secreting pituitary adenoma (AtT-20) cells. In addition, the antitumor activity of bromocriptine was inhibited both by actinomycin D and cycloheximide, suggesting that it was dependent on new RNA and protein synthesis. Interestingly, the results of DNA fragmentation assays and cell cycle analysis clearly demonstrated that bromocriptine induced apoptosis in AtT-20 cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenoma / metabolism
  • Adenoma / pathology*
  • Adrenocorticotropic Hormone / metabolism*
  • Animals
  • Antineoplastic Agents / pharmacology*
  • Apoptosis / drug effects*
  • Bromocriptine / pharmacology*
  • Cell Division / drug effects
  • DNA, Neoplasm / metabolism
  • Flow Cytometry
  • Mice
  • Pituitary Neoplasms / metabolism
  • Pituitary Neoplasms / pathology*
  • Protein Biosynthesis
  • RNA / biosynthesis
  • Tumor Cells, Cultured

Substances

  • Antineoplastic Agents
  • DNA, Neoplasm
  • Bromocriptine
  • RNA
  • Adrenocorticotropic Hormone