Abstract
Commensal microbiota has emerged as an essential biomarker and regulator of both tumorigenesis and response to cancer therapy. However, our current knowledge about microbiota in cancer has been largely limited to intestinal microbiota. As a mucosal organ harboring one of the largest surface areas in the body, the lung is exposed to a variety of microbes through inhalation and micro-aspiration, and is colonized by a diverse bacterial community in both physiological and pathological conditions. Importantly, increasing evidence has linked the lung microbiome to cancer development. Studies in lung cancer patients and mouse models have revealed tumor-associated dysregulation of the local microbiome in the lung, which in turn impacts cancer progression by shaping the tumor microenvironment and modulating the activity of tumor-infiltrating immune cells. These findings not only provide novel mechanistic insight into the biology of lung cancer but also shed light on new therapeutic targets and strategies for lung cancer prevention and treatment. The goal of this review is to discuss the key findings, remaining questions, and future directions in this new and exciting field.
Highlights
Mucosal surfaces exposed to the external environment are colonized by a vast number of microbes consisting of bacteria, viruses, fungi and archaea, which are collectively referred to as the commensal microbiota [1, 2]
As a number of bacterial metabolites have been implicated in the regulation of host metabolism and signaling pathways [41], it is possible that the alteration of bacteria-derived molecules resulting from dysbiosis in the tumor microenvironment can affect the metabolism and oncogenic signaling of lung cancer cells
Given that the intestinal microbiome is the main target of oral antibiotic treatment, these findings suggest that distal intestinal microbiota may indirectly regulate lung cancer development and the therapeutic efficacy of chemotherapy or immunotherapy through regulation of the systemic immune response
Summary
Mucosal surfaces exposed to the external environment are colonized by a vast number of microbes consisting of bacteria, viruses, fungi and archaea, which are collectively referred to as the commensal microbiota [1, 2]. Commensal microbiota was essential in maintaining host metabolic homeostasis, instructing the development of specific organ structures, and driving the maturation of the host. Dysregulation of the microbiota with altered bacterial composition, quantity, and diversity has been found to increase host susceptibility to various pathogen infections, exacerbate intestinal inflammation and autoimmunity, induce different forms of metabolic disorders, and promote the development of neurological diseases [5, 6]. Despite the recent development of targeted therapies for some genetic subtypes of human lung cancer, overall survival rates for this disease remain very low. Focusing on these key questions, we hereby summarize the recent advances in this rising area of host-microbiome interaction in lung cancer The critical questions are: does the lung have its own indigenous microbiota, and do the lung microbiota change with cancer? How do the microbiota impact lung carcinogenesis? What are the underlying mechanisms and any potential clinical implications? Focusing on these key questions, we hereby summarize the recent advances in this rising area of host-microbiome interaction in lung cancer
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