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ZNF750  is one novel significantly mutated gene identified in esophageal squamous cell carcinoma (ESCC) using next-generation sequencing. However, its clinically relevant and potential mechanisms have remained elusive. Using genomic sequencing of 612 ESCC patients, we analyzed the associations of  ZNF750  mutations with clinicopathologic features and its prognostic value. We further investigated the function and underlying mechanism of  ZNF750  in angiogenesis. The results showed  ZNF750  mutations/deletions are significantly associated with malignant progression and poor prognosis of ESCC patients. Decreased  ZNF750  in ESCC cells induces enhanced angiogenesis of human umbilical vein endothelial cells (HUVECs) and human arterial endothelial cells (HAECs), and the effect may be indirectly mediated by FOXC2. RNA-seq and ChIP shows lncRNA  DANCR  is a direct downstream target of  ZNF750 . Furtherly, knockdown  ZNF750  evokes  DANCR  expression, which prevents  miR-4707-3p  to interact with  FOXC2  as a microRNA sponge in a ceRNA manner, leading to enhanced FOXC2 signaling and angiogenesis. In contrast,  ZNF750  expression reverses the effect. Our study reveals a novel mechanism of  ZNF750 , highlights a significance of  ZNF750  as a metastatic and prognostic biomarker, and offers potential therapeutic targets for ESCC patients harboring  ZNF750  mutations.

Decreased ZNF750 promotes angiogenesis in a paracrine manner via activating DANCR/miR-4707-3p/FOXC2 axis in esophageal squamous cell carcinoma