已经有数据显示LINC01001在肺癌中高表达，但未报道M2巨噬细胞外泌体中LINC01001对非小细胞肺癌（NSCLC）中METTL3、糖酵解和免疫的影响。本研究旨在探讨M2巨噬细胞外泌体中LINC01001在NSCLC中的调控效应和机制。我们研究结果显示，在巨噬细胞外泌体验证后，证实外泌体调节了NSCLC细胞的增殖、葡萄糖摄取、乳酸产生和ATP水平。外泌体还促进了METTL3的表达。生物信息学筛选显示LINC01001调控了METTL3。随后的实验揭示外泌体中的LINC01001影响了NSCLC细胞的糖酵解过程。通过RIP，证明了LINC01001与METTL3结合发挥功能。生物信息学预测NASP是METTL3的靶向基因。LINC01001还能调控NASP的甲基化。小鼠的肿瘤发生也表明LINC01001介导了METTL3刺激肿瘤的发展。本研究成功验证了来自M2巨噬细胞外泌体中的LINC01001。证实LINC01001能与METTL3相互作用并调节NSCLC细胞的糖酵解过程。LINC01001还抑制了T细胞的增殖。© 2023. 作者，Springer Nature America, Inc. 独家许可。

There have been data showing that LINC01001 is highly expressed in lung cancer, but the effect of M2 macrophage exosomal LINC01001 to METTL3, glycolysis and immunity in non-small cell lung cancer (NSCLC) has not been reported. In this study, we aimed to explore the regulatory effect and mechanism of M2 macrophage exosomal LINC01001 in NSCLC. The results of our study show that the verification of macrophage exosomes, it was confirmed that exosomes regulated proliferation, glucose intake, lactate production and ATP levels of NSCLC cells. Exosomes also promoted the expression of METTL3. Bioinformatics screening showed that LINC01001 regulated METTL3. Subsequent experiments revealed exosomal LINC01001 influenced the glycolysis processes of NSCLC cells. Through RIP, it was proved that LINC01001 functioned in combination with METTL3. Bioinformatics predicted that NASP was a METTL3-targeted gene. LINC01001 could also regulate NASP methylation. Tumorigenesis in mice also indicated that LINC01001 mediated METTL3 to stimulate the development of tumors. In this study, LINC01001 was successfully verified in the exosomes-derived from M2 macrophages. It was confirmed that LINC01001 could interact with METTL3 and regulate glycolysis process in NSCLC cells. LINC01001 also inhibited T cell proliferation.© 2023. The Author(s), under exclusive licence to Springer Nature America, Inc.