Epidermal growth factor (EGF) signaling regulates multiple cellular processes and plays an essential role in tumorigenesis. Epiregulin (EREG), a member of the EGF family, binds to the epidermal growth factor receptor (EGFR) and ErbB4, and it stimulates EGFR-related downstream pathways. Increasing evidence indicates that both the aberrant expression and oncogenic function of EREG play pivotal roles in tumor development in many human cancers, including non-small cell lung cancer (NSCLC). EREG overexpression is induced by activating mutations in theEGFR,KRAS, andBRAFand contributes to the aggressive phenotypes of NSCLC with oncogenic drivers. Recent studies have elucidated the roles of EREG in a tumor microenvironment, including the epithelial–mesenchymal transition, angiogenesis, immune evasion, and resistance to anticancer therapy. In this review, we summarized the current understanding of EREG as an oncogene and discussed its oncogenic role in lung tumorigenesis and therapeutic resistance.
表皮生长因子（EGF）信号通路调控多种细胞过程，在肿瘤发生发展中发挥关键作用。表皮调节素（EREG）作为EGF家族成员，可与表皮生长因子受体（EGFR）及ErbB4结合，激活EGFR相关下游通路。越来越多的证据表明，EREG的异常表达及其致癌功能在包括非小细胞肺癌（NSCLC）在内的多种人类肿瘤发展中起核心作用。EGFR、KRAS和BRAF的激活突变可诱导EREG过表达，进而促进携带致癌驱动基因的NSCLC侵袭表型。最新研究揭示了EREG在肿瘤微环境中的多重作用，包括调控上皮-间质转化、血管生成、免疫逃逸及抗癌治疗耐药。本综述系统总结了当前对EREG致癌功能的认识，并深入探讨其在肺肿瘤发生及治疗耐药中的分子机制。
Role of Epiregulin in Lung Tumorigenesis and Therapeutic Resistance
肿瘤(癌症)患者之家