肺癌，尤其是非小细胞肺癌 (NSCLC)，占肺癌病例的80%以上，仍然是导致癌症死亡的主要原因，5年存活率低于20%。对该疾病发病机制的持续了解以及鉴定用于治疗及治疗反应的生物标记物将有助于改善患者的生存率。在本研究中，我们发现一种被称为DUSP10（也被称为MAPK磷酸酶5）的分子在非小细胞肺癌中具有致癌作用。NSCLC细胞中DUSP10的过表达导致ERK和JNK的活化降低，但p38的活化增加，这与细胞生长和迁移增加相关。当接种到免疫缺陷小鼠体内时，DUSP10过表达的NSCLC细胞形成的肿瘤比对照组细胞更大。DUSP10过表达的NSCLC细胞的增长增加与促肿瘤细胞因子（包括IL-6和TGFβ）的表达增加有关。重要的是，较高的DUSP10表达与NSCLC患者预后较差相关。因此，DUSP10可作为NSCLC预后的生物标记物，并可成为肺癌治疗方法开发的靶点。版权所有©2023年韩国免疫学会。

Lung cancer, particularly non-small cell lung cancer (NSCLC) which contributes more than 80% to totally lung cancer cases, remains the leading cause of cancer death and the 5-year survival is less than 20%. Continuous understanding on the mechanisms underlying the pathogenesis of this disease and identification of biomarkers for therapeutic application and response to treatment will help to improve patient survival. Here we found that a molecule known as DUSP10 (also known as MAPK phosphatase 5) is oncogenic in NSCLC. Overexpression of DUSP10 in NSCLC cells resulted in reduced activation of ERK and JNK, but increased activation of p38, which was associated with increased cellular growth and migration. When inoculated in immunodeficient mice, the DUSP10-overexpression NSCLC cells formed larger tumors compared to control cells. The increased growth of DUSP10-overexpression NSCLC cells was associated with increased expression of tumor-promoting cytokines including IL-6 and TGFβ. Importantly, higher DUSP10 expression was associated with poorer prognosis of NSCLC patients. Therefore, DUSP10 could severe as a biomarker for NSCLC prognosis and could be a target for development of therapeutic method for lung cancer treatment.Copyright © 2023. The Korean Association of Immunologists.