ArticleThe EMBO journal2009
The antiapoptotic protein AAC-11 interacts with and regulates Acinus-mediated DNA fragmentation.
Article in The EMBO journal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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48 citing papers in PubMed.
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- Peptides that immunoactivate the tumor microenvironment.Biochimica et biophysica acta. Reviews on cancer · 2021Review
- Efficient Therapeutic Delivery by a Novel Cell-Penetrating Peptide Derived from Acinus.Cancers · 2020Article
- Antiapoptotic Clone 11-Derived Peptides InduceJournal of virology · 2020Article
- Regulation of mRNA export through API5 and nuclear FGF2 interaction.Nucleic acids research · 2020Article
- Titanium Dioxide Nanoparticles Alter the Cellular Phosphoproteome in A549 Cells.Nanomaterials (Basel, Switzerland) · 2020Article
- Prophylactic and therapeutic antileukemic effects induced by the AAC-11-derived Peptide RT53.Oncoimmunology · 2020Article
- High expression of apoptosis protein (Api-5) in chemoresistant triple-negative breast cancers: an innovative target.Oncotarget · 2019Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The nuclear factor Acinus has been suggested to mediate apoptotic chromatin condensation after caspase cleavage. However, this role has been challenged by recent observations suggesting a contribution of Acinus in apoptotic internucleosomal DNA cleavage. We report here that AAC-11, a survival protein whose expression prevents apoptosis that occurs on deprivation of growth factors, physiologically binds to Acinus and prevents Acinus-mediated DNA fragmentation. AAC-11 was able to protect Acinus from caspase-3 cleavage in vivo and in vitro, thus interfering with its biological function. Interestingly, AAC-11 depletion markedly increased cellular sensitivity to anticancer drugs, whereas its expression interfered with drug-induced cell death. AAC-11 possesses a leucine-zipper domain that dictates, upon oligomerization, its interaction with Acinus as well as the antiapoptotic effect of AAC-11 on drug-induced cell death. A cell permeable peptide that mimics the leucine-zipper subdomain of AAC-11, thus preventing its oligomerization, inhibited the AAC-11-Acinus complex formation and potentiated drug-mediated apoptosis in cancer cells. Our results, therefore, show that targeting AAC-11 might be a potent strategy for cancer treatment by sensitization of tumour cells to chemotherapeutic drugs.
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