Implications of m6A methylation and microbiota interaction in non-small cell lung cancer: From basics to therapeutics

N6-methyladenine (m6A) is one of the most common RNA epigenetic modifications in all higher eukaryotes. Increasing evidence demonstrated that m6A-related proteins, acted as oncogenes or tumor suppressors, are abnormally expressed in the cell lines and tissues of non-small cell lung cancer (NSCLC). I...

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Main Authors: Fen-Sheng Qiu, Jia-Qi He, Yu-Sen Zhong, Mei-Ying Guo, Chen-Huan Yu
Format: Article
Language:English
Published: Frontiers Media S.A. 2022-09-01
Series:Frontiers in Cellular and Infection Microbiology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fcimb.2022.972655/full
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author Fen-Sheng Qiu
Jia-Qi He
Yu-Sen Zhong
Mei-Ying Guo
Chen-Huan Yu
Chen-Huan Yu
Chen-Huan Yu
author_facet Fen-Sheng Qiu
Jia-Qi He
Yu-Sen Zhong
Mei-Ying Guo
Chen-Huan Yu
Chen-Huan Yu
Chen-Huan Yu
author_sort Fen-Sheng Qiu
collection DOAJ
description N6-methyladenine (m6A) is one of the most common RNA epigenetic modifications in all higher eukaryotes. Increasing evidence demonstrated that m6A-related proteins, acted as oncogenes or tumor suppressors, are abnormally expressed in the cell lines and tissues of non-small cell lung cancer (NSCLC). In addition, lung as the special immune organ contacts with the outer environments and thereby inevitably suffers from different types of microbial pathogen attack. Those microbial pathogens affect the development, progression, and clinical outcomes of NSCLC via altering host m6A modification to disrupt pulmonary immune homeostasis and increase the susceptibility; conversely, host cells modulate m6A modification to repress bacterial colonization. Therefore, m6A harbors the potential to be the novel biomarkers and targets for predicting poor prognosis and chemotherapy sensitivity of patients with lung cancer. In this paper, we provided an overview of the biological properties of m6A-modifying enzymes, and the mechanistic links among lung microbiota, m6A modification and NSCLC. Although the flood of novel m6A-related inhibitors represents many dramatic improvements in NSCLC therapy, their efficacy and toxicity in NSCLC are explored to address these pivotal gaps in the field.
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spelling doaj.art-a69d56ff09b7438e8b441608491643812022-12-22T02:20:42ZengFrontiers Media S.A.Frontiers in Cellular and Infection Microbiology2235-29882022-09-011210.3389/fcimb.2022.972655972655Implications of m6A methylation and microbiota interaction in non-small cell lung cancer: From basics to therapeuticsFen-Sheng Qiu0Jia-Qi He1Yu-Sen Zhong2Mei-Ying Guo3Chen-Huan Yu4Chen-Huan Yu5Chen-Huan Yu6Key Laboratory of Experimental Animal and Safety Evaluation, Zhejiang Academy of Medical Sciences (Hangzhou Medical College), Hangzhou, ChinaPharmaceutical Department, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, ChinaKey Laboratory of Experimental Animal and Safety Evaluation, Zhejiang Academy of Medical Sciences (Hangzhou Medical College), Hangzhou, ChinaKey Laboratory of Experimental Animal and Safety Evaluation, Zhejiang Academy of Medical Sciences (Hangzhou Medical College), Hangzhou, ChinaKey Laboratory of Experimental Animal and Safety Evaluation, Zhejiang Academy of Medical Sciences (Hangzhou Medical College), Hangzhou, ChinaCancer Hospital of the University of Chinese Academy of Sciences (Zhejiang Cancer Hospital), Hangzhou, ChinaInstitute of Basic Medicine and Cancer, Chinese Academy of Sciences, Hangzhou, ChinaN6-methyladenine (m6A) is one of the most common RNA epigenetic modifications in all higher eukaryotes. Increasing evidence demonstrated that m6A-related proteins, acted as oncogenes or tumor suppressors, are abnormally expressed in the cell lines and tissues of non-small cell lung cancer (NSCLC). In addition, lung as the special immune organ contacts with the outer environments and thereby inevitably suffers from different types of microbial pathogen attack. Those microbial pathogens affect the development, progression, and clinical outcomes of NSCLC via altering host m6A modification to disrupt pulmonary immune homeostasis and increase the susceptibility; conversely, host cells modulate m6A modification to repress bacterial colonization. Therefore, m6A harbors the potential to be the novel biomarkers and targets for predicting poor prognosis and chemotherapy sensitivity of patients with lung cancer. In this paper, we provided an overview of the biological properties of m6A-modifying enzymes, and the mechanistic links among lung microbiota, m6A modification and NSCLC. Although the flood of novel m6A-related inhibitors represents many dramatic improvements in NSCLC therapy, their efficacy and toxicity in NSCLC are explored to address these pivotal gaps in the field.https://www.frontiersin.org/articles/10.3389/fcimb.2022.972655/fullepigeneticsbiomarkerMETTL3FTOinhibitorm6A
spellingShingle Fen-Sheng Qiu
Jia-Qi He
Yu-Sen Zhong
Mei-Ying Guo
Chen-Huan Yu
Chen-Huan Yu
Chen-Huan Yu
Implications of m6A methylation and microbiota interaction in non-small cell lung cancer: From basics to therapeutics
Frontiers in Cellular and Infection Microbiology
epigenetics
biomarker
METTL3
FTO
inhibitor
m6A
title Implications of m6A methylation and microbiota interaction in non-small cell lung cancer: From basics to therapeutics
title_full Implications of m6A methylation and microbiota interaction in non-small cell lung cancer: From basics to therapeutics
title_fullStr Implications of m6A methylation and microbiota interaction in non-small cell lung cancer: From basics to therapeutics
title_full_unstemmed Implications of m6A methylation and microbiota interaction in non-small cell lung cancer: From basics to therapeutics
title_short Implications of m6A methylation and microbiota interaction in non-small cell lung cancer: From basics to therapeutics
title_sort implications of m6a methylation and microbiota interaction in non small cell lung cancer from basics to therapeutics
topic epigenetics
biomarker
METTL3
FTO
inhibitor
m6A
url https://www.frontiersin.org/articles/10.3389/fcimb.2022.972655/full
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