ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2020
ILC3 cells promote the proliferation and invasion of pancreatic cancer cells through IL-22/AKT signaling.
Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 38 citations in OpenAlex.
- IDH1 Mutant Glioma Favors Group 3 Innate Lymphoid Cells and Is Resistant to Immune Checkpoint Expression.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Leukemia-driven expansion of type 3 innate lymphoid cell facilitates a pro-tumoral microenvironment in acute myeloid leukemia.Leukemia · 2026Article
- IL-20 Subfamily Biological Effects: Mechanistic Insights and Therapeutic Perspectives in Cancer.International journal of molecular sciences · 2025Review
- Article
- Innate immune cells in tumor microenvironment: A new frontier in cancer immunotherapy.iScience · 2024Review
- IL-22: A key inflammatory mediator as a biomarker and potential therapeutic target for lung cancer.Heliyon · 2024Review
- The role of IL-22 in cancer.Medical oncology (Northwood, London, England) · 2024Review
- Disease pathogenesis and barrier functions regulated by group 3 innate lymphoid cells.Seminars in immunopathology · 2024Review
- Bridging Chronic Inflammation and Digestive Cancer: The Critical Role of Innate Lymphoid Cells in Tumor Microenvironments.International journal of biological sciences · 2024Review
- The Roles of Innate Lymphoid Cells in the Gastric Mucosal Immunology and Oncogenesis of Gastric Cancer.International journal of molecular sciences · 2023Review
- The role of group 3 innate lymphoid cell in intestinal disease.Frontiers in immunology · 2023Review
- ILC3: a case of conflicted identity.Frontiers in immunology · 2023Review
- IL-22 regulates inflammatory responses to agricultural dust-induced airway inflammation.Toxicology and applied pharmacology · 2022Article
- Review
- Innate Lymphoid Cells: Emerging Players in Pancreatic Disease.International journal of molecular sciences · 2022Review
- Innate lymphoid cells and cancer.Nature immunology · 2022Review
- Th22 Cells/IL-22 Serves as a Protumor Regulator to Drive Poor Prognosis through the JAK-STAT3/MAPK/AKT Signaling Pathway in Non-Small-Cell Lung Cancer.Journal of immunology research · 2022Article
- Human ILC3 Exert TRAIL-Mediated Cytotoxicity Towards Cancer Cells.Frontiers in immunology · 2022Article
- Innate lymphoid cells type 3 in cancer.Frontiers in immunology · 2022Review
- Dysregulation of ILC3s unleashes progression and immunotherapy resistance in colon cancer.Cell · 2021Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
purposeType 3 innate lymphocytes (ILC3s) are reported to be involved in lung cancer, possibly by producing interleukin-22 (IL-22). However, whether ILC3s and their secreted IL-22 molecules contribute to the pathogenesis of pancreatic cancer (PC) remains unclear. To this end, in this study, we investigated the effects and possible mechanisms of ILC3s on PC pathogenesis.
methodThe IL-22 and IL-2i2R levels and the ILC3s' frequency in cancer tissues from PC patients and in peripheral blood from PC patients and healthy controls were analyzed by flow cytometry, immunochemistry, or immunofluorescence. The effects of IL-22-induced AKT signaling on the proliferation, invasion, and migration of PC cells were examined by co-culturing PC cell lines with ILC3s isolated from PC tissues, with or without the addition of neutralizing IL-22 antibody, IL-22R antibody or AKT inhibitor.
resultsOur results showed that IL-22 and ILC3s were significantly upregulated in the PBMCs and cancer tissues of PC patients, and the IL-22R level was increased in PC cells. The increased frequency of ILC3s was positively correlated with the clinical features of PC patients. Co-culture experiments indicated that ILC3s promoted the proliferation, invasion, and migration of PC cell lines by secreting IL-22 to activate AKT signaling because IL-22/IL-22R or AKT blockage markedly counteracted such effects on PC cells.
conclusionOur data demonstrated that ILC3s may promote PC pathogenesis through IL-22/IL-22R-AKT signaling, suggesting a potential intervention target for PC treatment in the future.
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