Abstract

The relationship between the microbiome and disease has been investigated for many years. As a highly malignant tumor, biomarkers for lung cancer are diverse. However, precision of these biomarkers has not yet been achieved. It has been confirmed that lung microecology changes in lung cancer patients compared with healthy individuals. Furthermore, the abundance of some bacterial species shows obvious changes, suggesting their potential use as a microbial marker for the detection of lung cancer. In addition, recent studies have confirmed that inflammation, immune response, virulence factors, and metabolism may be potential mechanisms linking the microbiome with carcinogenesis. In this review, microbiome studies of lung cancer, potential mechanisms, potential microbial markers, and the influence of the microbiome on the diagnosis and treatment of lung cancer are summarized, providing theoretical strategies for the diagnosis and treatment of lung cancer.

Highlights

  • In recent years, the relationship between the microbiome and disease has attracted wide attention

  • 859 genes were related to tumorigenesis and metastasis. These results suggested that inflammation-inducing factors in cigarette smoke can cause early epigenetic changes in the lung, which, together with other factors, can cause lung cancer [19]

  • Capnocytophaga, and Veillonella may be potential biomarkers of lung cancer [84]. Another metagenomic sequence analysis found that the abundance of Granulicatella adiacens, Streptococcus intermedius, S. viridans, and M. tuberculosis in the sputum of patients with lung cancer was significantly higher compared with the non-cancerous group

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Summary

Introduction

The relationship between the microbiome and disease has attracted wide attention. Microorganisms can promote the occurrence of lung cancer through inflammation, immune responses, virulence factors, and metabolism; inflammatory factors, such as interleukin (IL), tumor necrosis factor (TNF)-a, and cyclooxygenase (COX)-2, are closely related to carcinogenesis [12].

Results
Conclusion

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