<p>Lung cancer remains the leading cause of cancer-related mortality worldwide. Beyond established risk factors like smoking, the human microbiota—comprising complex communities in the gut, respiratory tract, oral cavity, and even within tumors—is increasingly recognized as a pivotal player in lung carcinogenesis, progression, and therapy response. This review synthesizes current evidence on the role of microecological dysbiosis in lung cancer. We detail how distinct microbial niches (gut, lower respiratory tract, oral, and intratumoral) contribute to pathogenesis through mechanisms including DNA damage, chronic inflammation, immune modulation, and metabolic interference. Furthermore, we examine the compelling role of the microbiota in mediating resistance to both chemotherapy and immunotherapy, highlighting how specific microbes can diminish or enhance treatment efficacy. Finally, we discuss the significant challenges in this field, such as microbial heterogeneity and establishing causality, and outline future directions. These include leveraging multi-omics integration, developing microbial biomarkers for diagnosis and prognosis, and exploring novel therapeutic strategies like microbiota modulation to improve patient outcomes. A deeper understanding of the lung cancer microbiome holds promise for revolutionizing prevention, diagnosis, and treatment paradigms.</p>

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The role and mechanisms of microecological dysbiosis in lung cancer therapy

  • You Shuai,
  • Min Tang

摘要

Lung cancer remains the leading cause of cancer-related mortality worldwide. Beyond established risk factors like smoking, the human microbiota—comprising complex communities in the gut, respiratory tract, oral cavity, and even within tumors—is increasingly recognized as a pivotal player in lung carcinogenesis, progression, and therapy response. This review synthesizes current evidence on the role of microecological dysbiosis in lung cancer. We detail how distinct microbial niches (gut, lower respiratory tract, oral, and intratumoral) contribute to pathogenesis through mechanisms including DNA damage, chronic inflammation, immune modulation, and metabolic interference. Furthermore, we examine the compelling role of the microbiota in mediating resistance to both chemotherapy and immunotherapy, highlighting how specific microbes can diminish or enhance treatment efficacy. Finally, we discuss the significant challenges in this field, such as microbial heterogeneity and establishing causality, and outline future directions. These include leveraging multi-omics integration, developing microbial biomarkers for diagnosis and prognosis, and exploring novel therapeutic strategies like microbiota modulation to improve patient outcomes. A deeper understanding of the lung cancer microbiome holds promise for revolutionizing prevention, diagnosis, and treatment paradigms.