p53-independent apoptosis induced by muscle differentiation stimuli in polyomavirus large T-expressing myoblasts

Vanesa Gottifredi, Angelo Peschiaroli, Gian Maria Fimia, Rossella Maione

Research output: Contribution to journalArticle


Abnormal proliferation signals, driven by cellular or viral oncogenes, can result in the induction of apoptosis under sub-optimal cell growth conditions. The tumor suppressor p53 plays a central role in mediating oncogene-induced apoptosis, therefore transformed cells lacking p53 are generally resistant to apoptosis-promoting treatments. In a previous work we have reported that the expression of polyomavirus large T antigen causes apoptosis in differentiating myoblasts and that this phenomenon is dependent on the onset of muscle differentiation in the absence of a correct cell cycle arrest. Here we report that polyomavirus large T increases the levels and activity of p53, but these alterations are not involved in the apoptotic mechanism. Apoptosis in polyomavirus large T-expressing myoblasts is not prevented by the expression of a p53 dominant-negative mutant nor it is increased by p53 over-expression. Moreover, forced differentiation induced through the over-expression of the muscle regulatory factor MyoD, leads to apoptosis without altering p53 function and, more significantly, even in a p53-null background. Our results indicate that apoptosis induced by the activation of muscle differentiation pathways in oncogene-expressing cells can occur in a p53-independent manner.

Original languageEnglish
Pages (from-to)2397-2407
Number of pages11
JournalJournal of Cell Science
Issue number14
Publication statusPublished - 1999


  • Apoptosis
  • Muscle differentiation
  • MyoD
  • p53
  • Polyomavirus large T

ASJC Scopus subject areas

  • Cell Biology

Fingerprint Dive into the research topics of 'p53-independent apoptosis induced by muscle differentiation stimuli in polyomavirus large T-expressing myoblasts'. Together they form a unique fingerprint.

  • Cite this