Age-related tumor growth in mice is related to integrin α 4 in CD8+ T cells
Open accessAbstract
Cancer incidence increases with age, but paradoxically, cancers have been found to grow more quickly in young mice compared with aged ones. The cause of differential tumor growth has been debated and, over time, attributed to faster tumor cell proliferation, decreased tumor cell apoptosis, and/or increased angiogenesis in young animals. Despite major advances in our understanding of tumor immunity over the past 2 decades, little attention has been paid to comparing immune cell populations in young and aged mice. Using mouse colon adenocarcinoma model MC38 implanted in young and mature mice, we show that age substantially influences the number of tumor-infiltrating cytotoxic CD8 + T cells, which control cancer progression. The different tumor growth pace in young and mature mice was abrogated in RAG1 null mice, which lack mature T and B lymphocytes, and upon selective depletion of endogenous CD8 + cells. Transcriptome analysis further indicated that young mice have decreased levels of the Itga4 gene (CD49d, VLA-4) in tumor-infiltrating lymphocytes when compared with mature mice. Hypothesizing that VLA-4 can have a tumor-protective effect, we depleted the protein, which resulted in accelerated tumor growth in mature mice. These observations may explain the paradoxical growth rates observed in murine cancers, point to the central role of VLA-4 in controlling tumor growth, and open new venues to therapeutic manipulation.
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In various mouse models, tumor proliferation is slower in elderly mice, such as MC38, B16, and 4T1 tumor models.
“In various mouse models, tumor proliferation was found to be slower in elderly mice, such as MC38, B16, and 4T1 tumor models [71].”
From Immunosenescence: a key player in cancer development (2020) · cites this paper as [71]
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BindingDB Entry 50020678: Design and Pharmacological Characterization of α
BindingDB (2024) · UC San Diego · doi:10.7270/q2pz5f9s
- Authors
- Oh, J., Magnuson, A., Benoist, C., Pittet, M. J., & Weissleder, R.
- Affiliations
- Massachusetts General Hospital (US)
- Brigham and Women's Hospital (US)
- Center for Systems Biology, Massachusetts General Hospital (MGH), Boston, Massachusetts, USA.
- Harvard University (US)
- Corresponding author
- Weissleder, Ralph
- Venue
- JCI Insight
- Published
- 2018-11-02
- Volume
- 3
- Issue
- 21
- ISSN
- 2379-3708 (ISSN-L)
- PMC
- PMC6238736
- OpenAlex
- W2898851664
- Cited by
- 51
- References
- 37
- Citations by year
- 2026: 3 · 2025: 12 · 2024: 8 · 2023: 6 · 2022: 8 · 2021: 4 · 2020: 8 · 2019: 2
- FWCI
- 1.31
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- JCI Insight (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Archive ouverte UNIGE (University of Geneva) (publishedVersion, other-oa)
- Funders
- National Cancer Institute (5T32CA079443-15)
- Topics
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
- Keywords
- aging, tumor growth, CD8+ T cells, CD49d, VLA-4, tumor-infiltrating lymphocytes, colon adenocarcinoma, MC38, Rag1 knockout, antitumor immunity, age-related cancer incidence
- MeSH terms
- Adenocarcinoma, Age Factors, Animals, Colonic Neoplasms, Female, Male, Mice, Inbred C57BL, Neoplasms, Experimental, T-Lymphocytes, Cytotoxic, Integrins, Lymphocytes, Tumor-Infiltrating, Homeodomain Proteins, CD8-Positive T-Lymphocytes, Gene Expression Profiling, Integrin alpha4beta1, Integrin alpha4, Cell Line, Tumor, Mice, Tumor Microenvironment
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