上皮间充质转化（EMT）是一种表现为细胞间接触减少的现象，与导致非小细胞肺癌（NSCLC）恶化和诱导转移有关。间隙蛋白 MAL 和与囊泡运输和膜连接域 3（MARVELD3）相关的蛋白是一种新型的紧密连接蛋白，参与了 EMT。对于 MARVELD3 在 NSCLC 中的机制了解非常有限。在这个试验中，将讨论 MARVELD3 对人类 NSCLC 细胞的抑制作用。测量了 NSCLC 组织和癌旁组织中 MARVELD3 的表达。检测了转化生长因子（TGF）-β1 诱导的 NSCLC 细胞中 MARVELD3 和 EMT 相关基因的表达。建立了 MARVELD3 消除和过表达的 NSCLC 细胞以分析 MARVELD3 与 EMT 和细胞迁移的关系。在 NSCLC 细胞模型和临床物种中，分析了 Wnt/β-连环蛋白通路的表达。在 NSCLC 样本中观察到的 MARVELD3 蛋白水平较癌旁标本低，并且 NSCLC 标本中 MARVELD3 的表达降低与肿瘤转移有关。TGF-β1 处理的 NSCLC 细胞中 E-Cadherin 和 MARVELD3 的表达降低，而 Vimentin 的表达增加。MARVELD3 改变了 EMT 相关基因并诱导了细胞迁移。此外，MARVELD3 过表达的 NSCLC 细胞中，Wnt/β-连环蛋白途径和靶基因 MYC 和 CCND1 的表达也受到抑制。MARVELD3 通过 Wnt/β-连环蛋白信号通路抑制了 TGF-β1 诱导的人类 NSCLC 细胞中的 EMT。这些结果表明，MARVELD3 可能成为 NSCLC 治疗中潜在的治疗方法。© 2023 作者。《胸部肿瘤》由中国肺癌专业委员会和澳大利亚约翰·威立出版有限公司出版。

The epithelial-mesenchymal transition (EMT), featured by abatement of cell-cell contact, is related to exacerbating non-small cell lung cancer (NSCLC) by inducing metastasis. MAL and relevant proteins for vesicle trafficking and membrane link domain 3 (MARVELD3) is a novel tight junction protein participated in the EMT. There is limited information available about the mechanism of MARVELD3 in NSCLC. In this trial, the inhibition effect of MARVELD3 on human NSCLC cells will be discussed.MARVELD3 expression was measured in NSCLC tissues and para-carcinoma tissues. The expression of MARVELD3 and EMT-related genes were examined in transforming growth factor (TGF)-β1-induced NSCLC cells. NSCLC cells with MARVELD3-knockdown and overexpressed were established to analyze the relationship between MARVELD3 and EMT and cell migration. The Wnt/β-catenin pathway expression was also analyzed in NSCLC cell models and clinic species.Lower protein levels of MARVELD3 were observed in NSCLC samples than para-carcinoma specimens, and the decreased expression of MARVELD3 in NSCLC specimens was associated with tumor metastasis. E-Cadherin and MARVELD3 expression was reduced in TGF-β1 treated NSCLC cells, whereas increased Vimentin expression was detected. MARVELD3 changed the EMT-related genes and induced cell migration. In addition, Wnt/β-catenin pathway and target genes, MYC and CCND1, expressions were inhibited in MARVELD3 overexpressed NSCLC cells.TGF-β1 induced EMT in human NSCLC cells can be suppressed by MARVELD3 through Wnt/β-catenin signaling pathway. These results indicate that MARVELD3 might be a potential therapeutic modality useful in the treatment of NSCLC.© 2023 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd.