Magmas overexpression inhibits staurosporine induced apoptosis in rat pituitary adenoma cell lines

PLoS One. 2013 Sep 17;8(9):e75194. doi: 10.1371/journal.pone.0075194. eCollection 2013.

Abstract

Magmas is a nuclear gene that encodes for the mitochondrial import inner membrane translocase subunit Tim16. Magmas is overexpressed in the majority of human pituitary adenomas and in a mouse ACTH-secreting pituitary adenoma cell line. Here we report that Magmas is highly expressed in two out of four rat pituitary adenoma cell lines and its expression levels inversely correlate to the extent of cellular response to staurosporine in terms of apoptosis activation and cell viability. Magmas over-expression in rat GH/PRL-secreting pituitary adenoma GH4C1 cells leads to an increase in cell viability and to a reduction in staurosporine-induced apoptosis and DNA fragmentation, in parallel with the increase in Magmas protein expression. These results indicate that Magmas plays a pivotal role in response to pro-apoptotic stimuli and confirm and extend the finding that Magmas protects pituitary cells from staurosporine-induced apoptosis, suggesting its possible involvement in pituitary adenoma development.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenoma / genetics*
  • Animals
  • Apoptosis / drug effects*
  • Apoptosis / genetics*
  • Caspase 3 / metabolism
  • Caspase 7 / metabolism
  • Cell Line, Tumor
  • Cell Proliferation
  • Cell Survival / drug effects
  • Cytochromes c / metabolism
  • Enzyme Activation / drug effects
  • Gene Expression*
  • Membrane Transport Proteins / genetics*
  • Mitochondria / drug effects
  • Mitochondria / metabolism
  • Mitochondrial Proteins / genetics*
  • Pituitary Neoplasms / genetics*
  • Rats
  • Staurosporine / pharmacology*

Substances

  • Magmas-ps1 protein, rat
  • Membrane Transport Proteins
  • Mitochondrial Proteins
  • Cytochromes c
  • Caspase 3
  • Caspase 7
  • Staurosporine

Grants and funding

This work was supported by the Italian Ministry of Education, Research and University (FIRB RBAP11884M and RBAP1153LS); Fondazione Cassa di Risparmio di Ferrara; and from Associazione Italiana per la Ricerca sul Cancro (AIRC). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.