FOXD1 Promotes Cell Growth and Metastasis by Activation of Vimentin in NSCLC.

摘要: Background/aims Forkhead box D1 (FOXD1) has a well-established role in early embryonic development and organogenesis functions as an oncogene several cancers. However, the clinical significance biological roles of FOXD1 non-small cell lung cancer (NSCLC) remain largely unknown. Methods A total 264 primary NSCLC tissue samples were collected. The expression levels these examined by immunohistochemical staining. was knocked down lentiviral shRNA. relative determined qRT-PCR, Western blotting immunofluorescence image. functional demonstrated viability CCK-8 assay, colony formation, invasion migration assays, apoptosis assay vitro. In vivo mouse xenograft metastasis models used to assess tumorigenicity metastatic ability. Chi-square test correlation between clinicopathological characteristics. Survival curves estimated Kaplan-Meier method compared using log-rank test. Cox proportional hazards model for univariate multivariate analyses. Results We that higher present tissues, especially tissues. also all cells with normal human bronchial epithelial cells. level associated malignant behavior poor prognosis patients. Knockdown significantly inhibited proliferation, migration, vitro tumor growth vivo, it increased rates Mechanistic analyses revealed expressed its oncogenic characteristics through activating Vimentin NSCLC. Multivariate regression analysis indicated independent prognostic factor both overall survival (OS) disease-free (DFS) Conclusion Our results might be involved progression oncogene, thereby potential therapeutic target