Abstract：
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.
摘要：
世界范围内NSCLC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)是发现在多种癌症中过表达的转录因子。然而,ETV5在NSCLC中的作用尚不清楚.我们旨在探讨ETV5在NSCLC发生发展中的作用和机制。在NSCLC组织和细胞系中评价ETV5的表达。根据ETV5的内源性表达建立ETV5过表达和下调细胞系。通过transwell测定进行功能研究。通过PCR阵列筛选ETV5的下游靶标，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。升高的ETV5表达通过TGFβ1的转录激活促进NSCLC细胞侵袭和迁移。因此,ETV5/TGFβ信号传导可以作为NSCLS患者的治疗靶标。
