非小细胞肺癌（NSCLC）是一种常见且具有侵袭性的恶性肿瘤，在全球范围内导致大量癌症相关死亡。解析调控NSCLC生长和转移的分子机制对于鉴定新的治疗靶点和开发有效的抗癌策略至关重要。一个值得关注的机制是METTL14的参与，METTL14是一种涉及多种细胞过程的RNA甲基转移酶，在NSCLC进展中发挥着作用。本研究的目标是调查METTL14在NSCLC发展和转移中的作用，并阐明其潜在的分子机制。通过了解METTL14对NSCLC发病机制的影响，本研究旨在为NSCLC治疗中的靶向治疗提供可能的途径。我们使用生物信息学和高通量转录组测序分析筛选影响NSCLC的调控机制。Kaplan-Meier方法评估了METTL14表达与NSCLC患者预后的相关性。通过克隆形成实验、流式细胞术、划痕实验和Transwell实验检查了操纵METTL14对NSCLC细胞恶性表型的影响。在裸鼠中评估了NSCLC细胞的肿瘤形成能力和转移潜能。METTL14在NSCLC组织和细胞系中过度表达。其高表达与NSCLC患者不良预后有关。METTL14沉默促进了NSCLC细胞的凋亡，并抑制了增殖、迁移和侵袭。miR-93-5p通过靶向和抑制TXNIP发挥作用。METTL14增加了miR-93-5p的表达，并通过m6A改变使pri-miR-93-5p成熟，以抑制TXNIP，从而抑制NSCLC细胞凋亡。通过控制miR-93-5p/TXNIP轴，METTL14增加了裸鼠中NSCLC细胞的肿瘤形成潜能和肺转移能力。本研究揭示了METTL14在NSCLC发展和转移中的作用，并将METTL14确定为NSCLC治疗的潜在靶点。© 2023. 作者独家授权给韩国基因学会。

Non-small cell lung cancer (NSCLC) is a prevalent and aggressive malignancy responsible for a significant number of cancer-related deaths worldwide. Unraveling the molecular mechanisms governing NSCLC growth and metastasis is crucial for the identification of novel therapeutic targets and the development of effective anti-cancer strategies. One such mechanism of interest is the involvement of METTL14, an RNA methyltransferase implicated in various cellular processes, in NSCLC progression.The objective of this study was to investigate the role of METTL14 in NSCLC development and metastasis and to elucidate the underlying molecular mechanisms. By understanding the impact of METTL14 on NSCLC pathogenesis, the study aimed to identify potential avenues for targeted therapies in NSCLC treatment.We used bioinformatics and high-throughput transcriptome sequencing analyses to screen regulatory mechanisms affecting NSCLC. The Kaplan-Meier method assessed the correlation between METTL14 expression and the prognosis of NSCLC patients. The effects of manipulated METTL14 on malignant phenotypes of NSCLC cells were examined by colony formation assay, flow cytometry, scratch assay, and Transwell assay. The tumorigenic capacity and metastatic potential of NSCLC cells in vivo were evaluated in nude mice.METTL14 was overexpressed in NSCLC tissues and cell lines. Its high expression indicated a poor prognosis for NSCLC patients. METTL14 silencing promoted apoptosis and repressed proliferation, migration, and invasion of NSCLC cells. miR-93-5p targeted and inhibited TXNIP. METTL14 increased miR-93-5p expression and matured pri-miR-93-5p through m6A alteration to inhibit TXNIP, thereby inhibiting NSCLC cell apoptosis. By controlling the miR-93-5p/TXNIP axis, METTL14 increased the tumorigenic potential and lung metastasis of NSCLC cells in nude mice.This study revealed a role for METTL14 in the contribution to NSCLC development and metastasis and identified METTL14 as a potential target for NSCLC treatment.© 2023. The Author(s) under exclusive licence to The Genetics Society of Korea.