肺癌是一个重要的公共健康问题，也是全球最常见的癌症相关死因。在真核生物中，G蛋白偶联受体（GPCR）家族是最大的一类膜蛋白群体。GPCR基因表达的改变和信号转导的失调已被认为是恶性的标志。作为GPCR家族的成员，G蛋白偶联受体37（GPR37）在肿瘤中的功能尚不明确，尤其是在非小细胞肺癌（NSCLC）中。 方法：我们通过TCGA、GTEx、GEO和GEPIA2探究了GPR37在NSCLC中的表达和预后。我们检测了NSCLC组织和细胞系中GPR37的表达。本研究探讨了GPR37对肿瘤细胞增殖的影响。此外，我们还检测了GPR37对肿瘤细胞凋亡和侵袭的影响。最重要的是，我们调查了GPR37是否影响NSCLC中顺铂诱导的药物抗性。此外，通过动物实验，我们评估了GPR37在NSCLC中的影响，并探讨了潜在机制。 （1）在NSCLC中，GPR37的表达明显高于相应的正常组织。我们发现高表达的GPR37预示着不良预后。 （2）研究表明，GPR37正调节NSCLC细胞的侵袭、迁移和增殖，抑制细胞凋亡，增强顺铂抗性，促进肿瘤形成和生长。相反，我们观察到GPR37的敲低抑制了NSCLC细胞的侵袭、迁移和增殖，促进细胞凋亡，增加对顺铂的敏感性，并影响肿瘤形成和生长。 （3）GPR37通过激活PI3K/Akt/mTOR信号转导途径来介导上皮间质转化（EMT），从而促进NSCLC的进展。这表明GPR37在促进NSCLC的发生和发展中起着关键作用。GPR37的敲除显著抑制了NSCLC的发生和发展。 因此，我们的研究结果表明，GPR37可能是NSCLC的一个可行的治疗靶点。 © 2023年作者。《癌症医学》由约翰·威利和子公司出版。

Lung cancer is a major public health concern and represents the most common cause of cancer-related death worldwide. Among eukaryotes, the G protein-coupled receptor (GPCR) family stands as the largest group of membrane proteins. Alterations in GPCR gene expression and dysregulation of signal transduction have been recognized as the markers of malignancy. As a member of the GPCR family, G protein-coupled receptor 37 (GPR37) exhibits unknown functions in tumors, particularly in non-small-cell lung cancer (NSCLC) METHODS: We explored the expression and prognosis of GPR37 in NSCLC through TCGA, GTEx, GEO, and GEPIA2. We detected the expression of GPR37 in NSCLC tissues and cell lines. The study explored the influence of GPR37 on tumor cell proliferation. Furthermore, we examined the effects of GPR37 on tumor cell apoptosis and invasion. Most importantly, we investigated whether GPR37 affects cisplatin-induced drug resistance in NSCLC. Furthermore, by conducting animal experiments, we assessed the impact of GPR37 on NSCLC and delved into underlying mechanisms.(1) In NSCLC, the expression of GPR37 is markedly higher than that in corresponding normal tissues. We found that elevated GPR37 expression predicts an unfavorable prognosis. (2) It was demonstrated that GPR37 positively regulates NSCLC cell invasion, migration, and proliferation, suppresses cell apoptosis, heightens resistance to cisplatin, and promotes tumor formation and growth. Conversely, we observed that GPR37 knockdown suppresses NSCLC cell invasion, migration, and proliferation, promotes cell apoptosis, increases sensitivity to cisplatin, and affects tumor formation and growth. (3) GPR37 activates PI3K/Akt/mTOR signal transduction pathways to mediate epithelial-mesenchymal transition (EMT), thereby promoting the progression of NSCLC.It was suggested that GPR37 acts a crucial role in promoting the occurrence and development of NSCLC. Knockdown of GPR37 significantly inhibits the occurrence and development of NSCLC. Therefore, our findings demonstrated that GPR37 may represent a viable therapeutic target for NSCLC.© 2023 The Authors. Cancer Medicine published by John Wiley & Sons Ltd.