肺癌是全球癌症相关发病率和死亡率的主要原因，其特点是侵袭性高、预后差。需要新的治疗靶点，特别是对于患有无法手术的转移性疾病的患者，需要全身治疗以改善患者的福利。最近的研究表明，TMEM176B是乳腺癌和胃癌的正调节因子，可能成为潜在的治疗靶点。在本研究中，我们利用单细胞测序、蛋白质组学、Co-IP以及体内和体外实验模型来研究TMEM176B在肺腺癌发展中的作用。我们的研究表明，TMEM176B 表达在肺腺癌组织中增强，并且与较短的总生存期 (OS) 相关。 TMEM176B 促进细胞功能，包括体外细胞增殖、侵袭、迁移和粘附以及体内肿瘤生长。此外，通过用肿瘤细胞条件培养基处理增强了内皮细胞的管形成能力。我们还证明 TMEM176B 通过 FGFR1/JNK/Vimentin/Snail 信号级联调节 EMT。总的来说，我们的研究表明 TMEM176B 可能是肺腺癌的潜在治疗靶点。

Lung cancer, the leading cause of cancer-related incidence and mortality worldwide, is characterised by high invasiveness and poor prognosis. Novel therapeutic targets are required, especially for patients with inoperable metastatic disease requiring systemic therapies to improve patients' welfare. Recently, studies indicated that TMEM176B is a positive regulator in breast and gastric cancers, and it could be a potential target for treatment. In this study, we used single-cell sequencing, proteomics, Co-IP, and in vivo and in vitro experimental models to investigate the role of TMEM176B in lung adenocarcinoma development. Our study indicated that TMEM176B expression was enhanced in lung adenocarcinoma tissues, and it was associated with shorter overall survival (OS). TMEM176B promoted cellular functions, including cell proliferation, invasion, migration and adhesion in vitro and tumour growth in vivo. Moreover, the tube formation ability of endothelial cells was enhanced by treating with the tumour cell-conditioned medium. We have also demonstrated that TMEM176B regulated EMT via the FGFR1/JNK/Vimentin/Snail signalling cascade. Overall, our study suggests TMEM176B could be a potential therapeutic target in lung adenocarcinoma.