YTHDF2抑制NSCLC发生、发展的相关分子机制  

Molecular Mechanism of YTHDF2 Inhibiting the Occurrence and Progression of NSCLC

作　　者：许浩然 刘浩然 徐汉林 靳春昊 温如然 胡晔 田凯华[1] 

机构地区：[1]青岛大学附属医院胸外科,山东 青岛 [2]青岛大学附属医院肿瘤科,山东 青岛 [3]青岛大学附属医院消化内科,山东 青岛 [4]青岛市第八人民医院肾病科,山东 青岛

出　　处：《临床医学进展》2025年第2期2041-2057,共17页Advances in Clinical Medicine

摘　　要：背景与目的:非小细胞肺癌(non-small cell lung cancer, NSCLC)是目前全球发病率最高和死亡人数最多的恶性肿瘤,而其具体的发病机制仍然未知。相关文献和既往实验研究发现m6A的阅读蛋白YTHDF2可能通过分子之间的相互作用抑制NSCLC的发生、发展。本研究拟通过对NSCLC患者肿瘤组织进行病理观察以及生信分析,探索NSCLC的发生发展机制,对未来产生更加有效的NSCLC治疗手段和改善NSCLC患者的预后提供参考。方法:回顾性收集2021年5月至2022年5月于青岛大学胸外科确诊肺癌并住院手术的64例NSCLC患者的肿瘤及癌旁组织(根据世界卫生组织形态学标准)。对上诉样本分别进行病理染色及生信分析。结果:64例标本的HE染色可见肿瘤组织中病理损伤明显,能明确采集样本的诊断并与癌旁组织区分。TUNEL染色可见:肿瘤组织细胞凋亡水平升高。qRT-PCR实验结果表明在肿瘤组织中YTHDF2和p14基因表达水平明显高于癌旁组织(P ARF蛋白的表达,达到延缓NSCLC发生、发展和改善NSCLC患者预后的作用。Background and objective: Non-small cell lung cancer (NSCLC) is currently the most prevalent and deadly malignancy worldwide. However, the precise mechanisms underlying its pathogenesis remain largely unknown. Previous literature and experimental studies suggest that YTHDF2, an m6A reader protein, may inhibit the initiation and progression of NSCLC through molecular interactions. This study aims to explore the mechanisms involved in the development and progression of NSCLC by conducting pathological observations and bioinformatic analyses of tumor tissues from NSCLC patients. The findings are expected to contribute to the development of more effective treatment strategies for NSCLC and to improve the prognosis of NSCLC patients. Methods: We retrospectively collected tumor and adjacent normal tissues from 64 NSCLC patients who were diagnosed and underwent surgery between May 2021 and May 2022 in the Depar

关 键 词：N6-甲基腺苷 YTH结构域连接蛋白2 非小细胞肺癌 机制 

分 类 号：R73[医药卫生—肿瘤]