ETV5 转录激活 TGFβ1，促进 NSCLC 癌细胞侵袭和迁移。
ETV5 transcriptionally activates TGFβ1 and promotes cancer cell invasion and migration of NSCLC.
机构信息
Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Department of Surgical Oncology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, China.
出版信息
J Mol Histol. 2023 Oct;54(5):419-426. doi: 10.1007/s10735-023-10148-3. Epub 2023 Sep 1.
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.
非小细胞肺癌（NSCLC）的发病率和死亡率在全球范围内仍然很高。然而，NSCLC 的分子机制在很大程度上仍不清楚。Ets 变体 5（ETV5）是一种转录因子，在多种癌症中发现过度表达。然而，ETV5 在 NSCLC 中的作用仍不清楚。我们旨在探讨 ETV5 在 NSCLC 发展中的作用和机制。评估了 ETV5 在 NSCLC 组织和细胞系中的表达。根据 ETV5 的内源性表达，建立了 ETV5 过表达和下调的细胞系。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验证。我们发现 ETV5 的过表达预示着 NSCLC 患者预后不良。升高的 ETV5 表达通过转录激活 TGFβ1 促进 NSCLC 细胞侵袭和迁移。因此，ETV5/TGFβ 信号通路可能成为 NSCLC 患者的治疗靶点。
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