ArticleInternational journal of medical sciences2025
Lung commensal bacteria promote lung cancer progression through NK cell-mediated immunosuppressive microenvironment.
Article in International journal of medical sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Intratumoral Microbiota in Lung Cancer: Emerging Roles in TME Modulation and Immunotherapy Response.International journal of molecular sciences · 2025Review
- The emerging role of microbiota in lung cancer: a new perspective on lung cancer development and treatment.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Lung microbiome dynamics in health and lung cancer.Microbial genomics · 2025Review
- Modulation of NK Cell Properties by ESKAPE Group Bacteria.International journal of molecular sciences · 2025Article
- Dissecting the intratumoral microbiome landscape in lung cancer.Frontiers in immunology · 2025Review
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Authors and funding
5 authors.
Funding
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Abstract
Symbiotic microbiota pervades the majority of the human body's organs and tissues, functioning as crucial regulators of both health maintenance and disease progression. Pertinently, lung adenocarcinoma has been indisputably linked to chronic inflammation. However, the precipitators that instigate such inflammation, along with the particular immune mediators involved, remain enigmatic and warrant extensive exploration. This research revealed a significant variance exists in the commensal bacteria between lung cancer tissues and their normal counterparts. This holds true for both clinical patients and mice, where both the diversity and abundance of bacteria in tumor tissues significantly surpass those in normal tissues. It has been demonstrated that disturbances in pulmonary commensal bacteria can stimulate the proliferation of tumor cells. Mechanistically, we suggest that lung bacteria may promote the expression of the NK cell immunosuppressive molecule TIGIT along with the secretion of IL-2 and IFN-γ. This consequently mediates alterations in the immunosuppressive microenvironment, thereby fostering tumor proliferation.
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