ArticleMolecular therapy. Nucleic acids2023
Overexpression of the mitochondrial anti-viral signaling protein, MAVS, in cancers is associated with cell survival and inflammation.
Article in Molecular therapy. Nucleic acids, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- MAVS as a Key Regulator of Tumor Proliferation, Survival, the Tumor Microenvironment, and Immunity.Biomolecules · 2026Article
- Old dogs-new tricks: multifaceted functions of MAVS beyond antivirus activity in human health and diseases.Cell & bioscience · 2025Review
- DUSP11 is an Intracellular Innate Immune Checkpoint in Lung Adenocarcinoma.Cancer immunology research · 2025Article
- Identification and Characterization of a Novel Rat MAVS Variant Modulating NFκB Signaling.Biomolecules · 2025Article
- MicroRNA-27b alleviates septic cardiomyopathy by targeting the Mff/MAVS axis.Frontiers in cellular and infection microbiology · 2025Article
- Elevated serum mtDNA in COVID-19 patients is linked to SARS-CoV-2 envelope protein targeting mitochondrial VDAC1, inducing apoptosis and mtDNA release.Apoptosis : an international journal on programmed cell death · 2024Article
- VDAC1-Based Peptides as Potential Modulators of VDAC1 Interactions with Its Partners and as a Therapeutic for Cancer, NASH, and Diabetes.Biomolecules · 2024Review
- Connection Between HIV and Mitochondria in Cardiovascular Disease and Implications for Treatments.Circulation research · 2024Review
- MAVS is a double-edged sword.Molecular therapy. Nucleic acids · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial anti-viral signaling protein (MAVS) plays an important role in host defense against viral infection via coordinating the activation of NF-κB and interferon regulatory factors. The mitochondrial-bound form of MAVS is essential for its anti-viral innate immunity. Recently, tumor cells were proposed to mimic a viral infection by activating RNA-sensing pattern recognition receptors. Here, we demonstrate that MAVS is overexpressed in a panel of viral non-infected cancer cell lines and patient-derived tumors, including lung, liver, bladder, and cervical cancers, and we studied its role in cancer. Silencing MAVS expression reduced cell proliferation and the expression and nuclear translocation of proteins associated with transcriptional regulation, inflammation, and immunity. MAVS depletion reduced expression of the inflammasome components and inhibited its activation/assembly. Moreover, MAVS directly interacts with the mitochondrial protein VDAC1, decreasing its conductance, and we identified the VDAC1 binding site in MAVS. Our findings suggest that MAVS depletion, by reducing cancer cell proliferation and inflammation, represents a new target for cancer therapy.
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