Cancer reports (Hoboken, N.J.) · 2025
m6A-Mediated Methylation Patterns and Their Association With Obstructive Sleep Apnea in Lung Adenocarcinoma.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Xia Lei, Chai Zhuodong, Wei Xiaoying, Wei Yuan, Zeng Daxiong, Jiang Junhong, Li Jing
Аннотация
BACKGROUND: Epigenetic regulation significantly affects immune responses in lung adenocarcinoma (LUAD). However, the role of RNA N6-methyladenosine (m6A) modification, especially in obstructive sleep apnea-hypopnea syndrome (OSAHS) within LUAD, is not well understood.
METHODS: This study examined m6A modification patterns in 973 LUAD patients using 23 regulatory genes. Unsupervised clustering categorized patients by m6A profiles, quantified by an m6A score. Associations with clinical outcomes, including survival, immune infiltration, tumor microenvironment, OSAHS incidence, and drug sensitivity, were analyzed.
RESULTS: m6A regulator mutations were linked to LUAD, revealing two distinct modification patterns and three gene clusters, all tied to immune phenotypes and clinical outcomes. Higher m6A scores correlated with lower survival, more frequent OSAHS, and increased immune activity. Patients with high m6A scores were more sensitive to PD-L1/PD-1 inhibitors and Phenformin, while those with low scores responded better to Cisplatin, Epothilone B, and Talazoparib.
CONCLUSION: Analyses confirmed m6A modification's role in LUAD progression, immune regulation, and outcomes. The m6A score is a valuable prognostic marker associated with survival, OSAHS incidence, and drug sensitivity. These findings highlight m6A's potential as a therapeutic target and biomarker, particularly for LUAD patients with OSAHS.
METHODS: This study examined m6A modification patterns in 973 LUAD patients using 23 regulatory genes. Unsupervised clustering categorized patients by m6A profiles, quantified by an m6A score. Associations with clinical outcomes, including survival, immune infiltration, tumor microenvironment, OSAHS incidence, and drug sensitivity, were analyzed.
RESULTS: m6A regulator mutations were linked to LUAD, revealing two distinct modification patterns and three gene clusters, all tied to immune phenotypes and clinical outcomes. Higher m6A scores correlated with lower survival, more frequent OSAHS, and increased immune activity. Patients with high m6A scores were more sensitive to PD-L1/PD-1 inhibitors and Phenformin, while those with low scores responded better to Cisplatin, Epothilone B, and Talazoparib.
CONCLUSION: Analyses confirmed m6A modification's role in LUAD progression, immune regulation, and outcomes. The m6A score is a valuable prognostic marker associated with survival, OSAHS incidence, and drug sensitivity. These findings highlight m6A's potential as a therapeutic target and biomarker, particularly for LUAD patients with OSAHS.