Background: Radiation-induced bystander effects (RIBE) increase the complexity of radiation therapy (RT). m6A modification is implicated in ionizing radiation damage. This study aims to investigate the RIBE and the mechanism after promoting m6A modification. Methods: Lung adenocarcinoma cells were treated to simulate a hypoxic and 0.5 Gy RT environment. The expression levels of METTL3, METTL14, and YTDHF2 were quantified by RT-qPCR. Paracellular clonogenicity and the expression of 53BP1 and gamma-H2AX were assessed by immunofluorescence. The proliferative rate was evaluated by CCK-8. Probes were employed to measure ROS levels. Micronucleus formation was evaluated microscopically. m6A-mRNA/lncRNA microarrays, MERIP-PCR, RT-qPCR, and ELISA were utilized to assess m6A modification levels and the expression of inflammatory factors. Results: m6A modification levels were significantly diminished under hypoxic, low-dose irradiation conditions. The overexpression of METTL3 in irradiated cancer cells resulted in increased clonogenicity and proliferation of paracellular cells, suppressed the rate of micronucleus formation, and reduced DNA damage by modulating the inflammatory response. m6A-mRNA/lncRNA microarray analyses revealed a higher correlation of inflammatory molecules NF-kappa B and TRAF6. Further analysis demonstrated that the m6A modification levels of inflammationrelated factors such as IL-6, TLR4, NF-kappa B2, and TRAF6 were significantly up-regulated, while their mRNA expression levels were notably decreased. Additionally, the expression of IL-10 and TGF-(3 was significantly reduced, with no significant changes observed in IL-1 expression. Conclusion: The overexpression of METTL3 facilitated m6A modification and mitigated the inflammatory response, thereby promoting paracellular cloning and proliferation, inhibiting micronucleus formation, alleviating DNA damage, and achieving the objective of suppression of RIBE.