Apollon gene silencing induces apoptosis in breast cancer cells through p53 stabilisation and caspase-3 activation

A. Lopergolo, M. Pennati, P. Gandellini, N. I. Orlotti, P. Poma, M. G. Daidone, M. Folini, N. Zaffaroni

Research output: Contribution to journalArticlepeer-review


We analysed the effects of small interfering RNA (siRNA)-mediated silencing of Apollon, a member of the inhibitors of apoptosis protein family, on the proliferative potential and ability of human breast cancer cell lines to undergo apoptosis. In wild-type p53 ZR75.1 cells, Apollon knockdown resulted in a marked, time-dependent decline of cell growth and an increased rate of apoptosis, which was associated with p53 stabilisation and activation of the mitochondrial-dependent apoptotic pathway. Pre-incubation of cells with a p53-specific siRNA resulted in a partial rescue of cell growth inhibition, as well as in a marked reduction of the apoptotic response, indicating p53 as a major player in cell growth impairment consequent on Apollon silencing. Apollon knockdown induced consistently less pronounced anti-proliferative and pro-apoptotic effects in mutant p53 MDA-MB-231 cells than in ZR75.1 cells. Furthermore, the activation of caspase-3 seemed to be essential for the induction of apoptosis after Apollon knockdown, as the Apollon-specific siRNA had no effect on the viability of caspase-3-deficient, wild-type p53 MCF-7 cells or the ZR75.1 cells after RNA interference-mediated caspase-3 silencing. Our results indicate that p53 stabilisation and caspase-3 activation concur to determine the apoptotic response mediated by Apollon knockdown in breast cancer cells, and suggest Apollon to be a potential new therapeutic target for this malignancy.

Original languageEnglish
Pages (from-to)739-746
Number of pages8
JournalBritish Journal of Cancer
Issue number5
Publication statusPublished - Mar 10 2009


  • Apollon
  • Apoptosis
  • Caspase-3
  • Human breast cancer
  • p53
  • siRNA

ASJC Scopus subject areas

  • Cancer Research
  • Oncology


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