Apaf-1 and caspase-9 do not act as tumor suppressors in myc-induced lymphomagenesis or mouse embryo fibroblast transformation

Clare L. Scott, Martin Schuler, Vanessa S. Marsden, Alex Egle, Marc Pellegrini, Dobrila Nesic, Steve Gerondakis, Stephen L. Nutt, Douglas R. Green, Andreas Strasser

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Abstract

Based on experiments with cultured fibroblasts, the apoptosis regulators caspase-9 and Apaf-1 are hypothesized to function as tumor suppressors. To investigate their in vivo role in lymphomagenesis, an IgH enhancer-driven c-myc transgene was crossed onto Apaf-1-/- and caspase-9-/- mice. Due to perinatal lethality, Eμ-myc transgenic Apaf-1-/- or caspase-9-/- fetal liver cells were used to reconstitute lethally irradiated recipient mice. Surprisingly, no differences were seen in rate, incidence, or severity of lymphoma with loss of Apaf-1 or caspase-9, and Apaf-1 was not a critical determinant of anticancer drug sensitivity of c-myc-induced lymphomas. Moreover, loss of Apaf-1 did not promote oncogene-induced transformation of mouse embryo fibroblasts. Thus, Apaf-1 and caspase-9 do not suppress c-myc-induced lymphomagenesis and embryo fibroblast transformation.

Original languageEnglish
Pages (from-to)89-96
Number of pages8
JournalJournal of Cell Biology
Volume164
Issue number1
DOIs
Publication statusPublished - 1 Jan 2004
Externally publishedYes

Keywords

  • Apaf-1
  • Apoptosis
  • Bcl-2
  • Cancer
  • Caspase

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