本研究旨在阐明LINC01006的N6-甲基腺苷（m6A）修饰参与非小细胞肺癌（NSCLC）的迁移、侵袭和增殖。在TCGA-LUAD队列中分析LINC01006和METTL3的表达。通过集落形成实验、伤口愈合实验和Transwell实验评价集落形成、迁移和侵袭的能力。 Q-PCR 和蛋白质印迹分析确定基因表达。 M6A-RNA 免疫沉淀和 m6A 定量测定用于评估 m6A 修饰。 qChIP 测定用于验证转录靶标。荧光素酶测定验证了 miRNA 靶标和转录靶标。采用原位异种移植模型来评估体内肿瘤增殖。LINC01006和METTL3在NSCLC细胞和组织中表达升高。 LINC01006通过上皮-间质转化（EMT）促进NSCLC的迁移和侵袭。 LINC01006的表达与METTL3的表达呈正相关。 METTL3在NSCLC原位异种移植模型中促进肿瘤形成和增殖。 METTL3 通过 m6A 修饰增加了 LINC01006 的表达。 c-MYC直接诱导METTL3。 c-MYC 和 LINC01006 共同被 miR-34a/b/c 和 miR-2682 靶向，因此 c-MYC/METTL3/LINC01006 通过 NSCLC 中的 miRNA 靶点形成正反馈环。LINC01006 是一种致癌 lncRNA，可诱导NSCLC的迁移、侵袭和增殖。 METTL3 通过稳定 LINC01006 mRNA 来增加 LINC01006 表达。 c-MYC 作为转录因子，激活 METTL3，从而导致 LINC01006 水平升高。 c-MYC、METTL3 和 LINC01006 通过 NSCLC 中的多个 miRNA 靶标形成正反馈环。版权所有 © 2023 作者。由 Elsevier B.V. 出版。保留所有权利。

This study aims to clarify the N6-methyladenosine (m6A) modification of LINC01006, which is involved in migration, invasion and proliferation of non-small cell lung cancer (NSCLC).LINC01006 and METTL3 expressions were analyzed in TCGA-LUAD cohort. Colony formation assay, wound-healing assay and transwell assay were performed to evaluate the ability of colony formation, migration and invasion. Q-PCR and western blot analysis determined gene expressions. M6A-RNA immunoprecipitation and m6A quantification assay were used to evaluate m6A modification. qChIP assay was used to validate transcriptional target. Luciferase assay validated the miRNA targets and transcriptional targets. In-situ xenograft model were included to evaluate tumor proliferation in vivo.LINC01006 and METTL3 expressions were elevated in NSCLC cells and tissues. LINC01006 promoted the migration and invasion of NSCLC via epithelial - mesenchymal transition (EMT). The expression of LINC01006 was positively correlated to the expression of METTL3. METTL3 promoted tumor formation and proliferation in the in-situ xenograft model of NSCLC. The expression of LINC01006 was increased by METTL3 via m6A modification. c-MYC directly induced METTL3. Both c-MYC and LINC01006 were commonly targeted by miR-34a/b/c and miR-2682, and thereby c-MYC/METTL3/LINC01006 formed a positive feedback loop through miRNA targets in NSCLC.LINC01006 is an oncogenic lncRNA, which induces migration, invasion and proliferation of NSCLC. METTL3 increases LINC01006 expression through stabilizing LINC01006 mRNA. c-MYC, as a transcription factor, activates METTL3, which results in an elevated level of LINC01006. c-MYC, METTL3 and LINC01006 form a positive feedback loop through multiple miRNA targets in NSCLC.Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.