Anticancer compound ABT-263 accelerates apoptosis in virus-infected cells and imbalances cytokine production and lowers survival rates of infected mice
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ABT-263 and its structural analogues ABT-199 and ABT-737 inhibit B-cell lymphoma 2 (Bcl-2), BCL2L1 long isoform (Bcl-xL) and BCL2L2 (Bcl-w) proteins and promote cancer cell death. Here, we show that at non-cytotoxic concentrations, these small molecules accelerate the deaths of non-cancerous cells infected with influenza A virus (IAV) or other viruses. In particular, we demonstrate that ABT-263 altered Bcl-xL interactions with Bcl-2 antagonist of cell death (Bad), Bcl-2-associated X protein (Bax), uveal autoantigen with coiled-coil domains and ankyrin repeats protein (UACA). ABT-263 thereby activated the caspase-9-mediated mitochondria-initiated apoptosis pathway, which, together with the IAV-initiated caspase-8-mediated apoptosis pathway, triggered the deaths of IAV-infected cells. Our results also indicate that Bcl-xL, Bcl-2 and Bcl-w interact with pattern recognition receptors (PRRs) that sense virus constituents to regulate cellular apoptosis. Importantly, premature killing of IAV-infected cells by ABT-263 attenuated the production of key pro-inflammatory and antiviral cytokines. The imbalance in cytokine production was also observed in ABT-263-treated IAV-infected mice, which resulted in an inability of the immune system to clear the virus and eventually lowered the survival rates of infected animals. Thus, the results suggest that the chemical inhibition of Bcl-xL, Bcl-2 and Bcl-w could potentially be hazardous for cancer patients with viral infections.
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ABT-263 sensitises retinal pigment epithelium cells and macrophages infected with influenza, herpes simplex, or measles to undergo cell death.
“Interestingly, ABT‐263 has been shown to sensitise retinal pigment epithelium cells and macrophages infected with a variety of virus types (influenza, herpes simplex, measles) to undergo cell death (Kakkola et al, 2013).”
From The struggle of a good friend getting old: cellular senescence in viral responses and therapy (2021) · cites this paper as Kakkola et al, 2013
Senolytic drugs can eliminate p16-positive macrophages and senescent vascular cells, exerting a dual approach to reverse vascular remodelling.
“Senolytic drugs can eliminate p16-positive macrophages 85 and senescent vascular cells, exerting a dual approach to reverse vascular remodelling.”
From The costs and benefits of senotherapeutics for human health (2022) · cites this paper as [85]
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Killing in self-defense: proapoptotic drugs to eliminate intracellular pathogens
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- Authors
- Kakkola, L., Denisova, O. V., Tynell, J., Viiliäinen, J., Ysenbaert, T., Matos, R. C., Nagaraj, A., Öhman, T., Kuivanen, S., Paavilainen, H., Feng, L., Yadav, B., Julkunen, I., Vapalahti, O., Hukkanen, V, Stenman, J., Aittokallio, T., Verschuren, E. W., Ojala, P. M., Nyman, T., Saelens, X., Dzeyk, K., & Kainov, D. E.
- Affiliations
- Institute for Molecular Medicine Finland (FI)
- Finnish Institute for Health and Welfare (FI)
- University of Helsinki (FI)
- Vlaams Instituut voor Biotechnologie (BE)
- University of Turku (FI)
- Minerva Foundation (FI)
- European Molecular Biology Laboratory (DE)
- Corresponding author
- Kainov, D E
- ORCID
- Venue
- Cell Death & Disease
- Published
- 2013-07-25
- Volume
- 4
- Issue
- 7
- Pages
- e742-e742
- ISSN
- 2041-4889 (ISSN-L)
- PMC
- PMC3730437
- OpenAlex
- W1966475300
- Cited by
- 54
- References
- 38
- Citations by year
- 2026: 3 · 2025: 6 · 2023: 1 · 2022: 8 · 2021: 8 · 2020: 11 · 2019: 3 · 2018: 3 · 2017: 2 · 2016: 5 · 2015: 2 · 2014: 2
- FWCI
- 1.34
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by-nc-sa
- www.springer.com/tdm (unspecified)
- Locations
- Cell Death and Disease (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Ghent University Academic Bibliography (Ghent University) (submittedVersion)
- Työväentutkimus Vuosikirja (submittedVersion)
- STM:n Hallinnonalan avoin julkaisuarkisto (Julkari) (submittedVersion)
- Funders
- Academy of Finland (255780)
- Jane ja Aatos Erkon Säätiö
- Kansainvälisen Liikkuvuuden ja Yhteistyön Keskus
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Health Sciences › Medicine › Epidemiology › Influenza Virus Research Studies
- Health Sciences › Medicine › Pharmacology › Flavonoids in Medical Research
- Keywords
- navitoclax, Bcl-2 family proteins, Bcl-xL, Bcl-w, influenza A virus, virus-infected cells, apoptosis, caspase-9, caspase-8, pattern recognition receptors, cytokine imbalance, antiviral immunity, Bax
- MeSH terms
- Aniline Compounds, Animals, Antineoplastic Agents, Disease Models, Animal, Macrophages, Neoplasms, Orthomyxoviridae Infections, Influenza A virus, Sulfonamides, Cytokines, Apoptosis, Cell Line, Tumor, Mice
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