pRb/E2F-1-mediated caspase-dependent induction of Noxa amplifies the apoptotic effects of the Bcl-2/Bcl-xL inhibitor ABT-737

Cell Death Differ. 2013 May;20(5):755-64. doi: 10.1038/cdd.2013.6. Epub 2013 Feb 22.

Abstract

Although Bcl-2 family members control caspase activity by regulating mitochondrial permeability, caspases can, in turn, amplify the apoptotic process upstream of mitochondria by ill-characterized mechanisms. We herein show that treatment with a potent inhibitor of Bcl-2 and Bcl-xL, ABT-737, triggers caspase-dependent induction of the BH3-only protein, Mcl-1 inhibitor, Noxa. RNA interference experiments reveal that induction of Noxa, and subsequent cell death, rely not only on the transcription factor E2F-1 but also on its regulator pRb. In response to ABT-737, pRb is cleaved by caspases into a p68Rb form that still interacts with E2F-1. Moreover, pRb occupies the noxa promoter together with E2F-1, in a caspase-dependent manner upon ABT-737 treatment. Thus, caspases contribute to trigger the mitochondrial apoptotic pathway by coupling Bcl-2/Bcl-xL inhibition to that of Mcl-1, via the pRb/E2F-1-dependent induction of Noxa.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects*
  • Apoptosis Regulatory Proteins / genetics
  • Biphenyl Compounds / pharmacology*
  • Breast Neoplasms
  • Caspases / metabolism
  • Cell Line, Tumor
  • DNA-Binding Proteins / genetics
  • E2F1 Transcription Factor / genetics
  • E2F1 Transcription Factor / metabolism*
  • Female
  • Humans
  • Mitochondria / metabolism
  • Mitochondrial Membrane Transport Proteins
  • Myeloid Cell Leukemia Sequence 1 Protein
  • Nitrophenols / pharmacology*
  • Nuclear Proteins / genetics
  • Piperazines / pharmacology
  • Promoter Regions, Genetic
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors
  • Proto-Oncogene Proteins c-bcl-2 / genetics
  • Proto-Oncogene Proteins c-bcl-2 / metabolism*
  • RNA Interference
  • RNA, Small Interfering
  • Retinoblastoma Protein / genetics
  • Retinoblastoma Protein / metabolism*
  • Sulfonamides / pharmacology*
  • Transcription, Genetic
  • Tumor Protein p73
  • Tumor Suppressor Proteins / genetics
  • bcl-2-Associated X Protein / antagonists & inhibitors
  • bcl-2-Associated X Protein / genetics
  • bcl-2-Associated X Protein / metabolism
  • bcl-X Protein / antagonists & inhibitors
  • bcl-X Protein / genetics
  • bcl-X Protein / metabolism

Substances

  • ABT-737
  • Apoptosis Regulatory Proteins
  • BAX protein, human
  • BBC3 protein, human
  • BCL2L1 protein, human
  • Biphenyl Compounds
  • DNA-Binding Proteins
  • E2F1 Transcription Factor
  • Mitochondrial Membrane Transport Proteins
  • Myeloid Cell Leukemia Sequence 1 Protein
  • Nitrophenols
  • Nuclear Proteins
  • PMAIP1 protein, human
  • Piperazines
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • RNA, Small Interfering
  • RTL10 protein, human
  • Retinoblastoma Protein
  • Sulfonamides
  • Tumor Protein p73
  • Tumor Suppressor Proteins
  • bcl-2-Associated X Protein
  • bcl-X Protein
  • Caspases