The morbidity and mortality of NSCLC remains high worldwide. However, the molecular mechanisms of NSCLC still largely unclear. Ets variant 5 (ETV5) is a transcription factor that found to be overexpressed in multiple cancers. However, the role of ETV5 in NSCLC remains unknown. We aim to explore the role and mechanisms of ETV5 in NSCLC development. The expression of ETV5 was evaluated in NSCLC tissues and cell lines. ETV5 overexpressing and downregulation cell lines were established according to the endogenous expression of ETV5. Functional studies were performed by transwell assay. The downstream targets of ETV5 were screened by PCR array and were confirmed by luciferase reporter assay. We found that overexpression of ETV5 indicates worse prognosis of NSCLC patients. Elevated ETV5 expression promotes NSCLC cell invasion and migration via transcriptional activates of TGFβ1. Therefore, ETV5/TGFβ signaling may serve as a therapeutic target for NSCLS patients.

全球非小细胞肺癌的发病率和死亡率仍然很高。然而，NSCLC的分子机制仍不清楚。Ets 变体 5 (ETV5) 是一种转录因子，被发现在多种癌症中过度表达。然而，ETV5 在 NSCLC 中的作用仍不清楚。我们的目的是探讨ETV5在NSCLC发展中的作用和机制。在 NSCLC 组织和细胞系中评估了 ETV5 的表达。根据ETV5内源表达情况建立ETV5过表达和下调细胞系。通过transwell测定进行功能研究。ETV5的下游靶标通过PCR阵列进行筛选，并通过荧光素酶报告基因测定进行确认。我们发现ETV5的过度表达表明NSCLC患者的预后较差。ETV5 表达升高通过 TGFβ1 转录激活促进 NSCLC 细胞侵袭和迁移。因此，ETV5/TGFβ信号传导可能作为NSCLS患者的治疗靶点。