ArticleFrontiers in pharmacology2022
Cell cycle block by p53 activation reduces SARS-CoV-2 release in infected alveolar basal epithelial A549-hACE2 cells.
Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 11 citations in OpenAlex.
- SARS-CoV-2 and Cancer Biology: Exploring the Mechanistic Links.Cancer reports (Hoboken, N.J.) · 2026Review
- Hyperglycemia-Induced Endothelial Dysfunction: From Classical Pathogenetic Mechanisms to Emerging Insights into ACE2 Protective Action.International journal of molecular sciences · 2026Review
- Synthetic Integration of an FCS into Coronaviruses-Hype or an Unresolved Biorisk? An Integrative Analysis of DNA Repair, Cancer Research, Drug Development, and Escape Mutant Traits.Life (Basel, Switzerland) · 2026Article
- Article
- Losartan and enalapril maleate differently influence SARS-CoV-2-infected vero cells.Scientific reports · 2024Article
- P53-Independent G1-Cell Cycle Arrest Increases SARS-CoV-2 RNA Replication.Microorganisms · 2024Article
- APOBEC3G Is a p53-Dependent Restriction Factor in Respiratory Syncytial Virus Infection of Human Cells Included in the p53/Immune Axis.International journal of molecular sciences · 2023Article
- Cell-Dependent Activation of ProTide Prodrugs and Its Implications in Antiviral Studies.ACS pharmacology & translational science · 2023Article
- Review
- Roles of p53-Mediated Host-Virus Interaction in Coronavirus Infection.International journal of molecular sciences · 2023Review
- Ganoderic Acid A and Its Amide Derivatives as Potential Anti-Cancer Agents by Regulating the p53-MDM2 Pathway: Synthesis and Biological Evaluation.Molecules (Basel, Switzerland) · 2023Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SARS-CoV viruses have been shown to downregulate cellular events that control antiviral defenses. They adopt several strategies to silence p53, key molecule for cell homeostasis and immune control, indicating that p53 has a central role in controlling their proliferation in the host. Specific actions are the stabilization of its inhibitor, MDM2, and the interference with its transcriptional activity. The aim of our work was to evaluate a new approach against SARS-CoV-2 by using MDM2 inhibitors to raise p53 levels and activate p53-dependent pathways, therefore leading to cell cycle inhibition. Experimental setting was performed in the alveolar basal epithelial cell line A549-hACE2, expressing high level of ACE2 receptor, to allow virus entry, as well as p53 wild-type. Cells were treated with several concentrations of Nutlin-3 or RG-7112, two known MDM2 inhibitors, for the instauration of a cell cycle block steady-state condition before and during SARS-CoV-2 infection, and for the evaluation of p53 activation and impact on virus release and related innate immune events. The results indicated an efficient cell cycle block with inhibition of the virion release and a significant inhibition of IL-6, NF-kB and IFN-λ expression. These data suggest that p53 is an efficient target for new therapies against the virus and that MDM2 inhibitors deserve to be further investigated in this field.
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