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Angiogenesis plays an important role in tumor growth and metastasis and has been reported to be inversely correlated with overall survival of osteosarcoma patients. It has been shown that apurinic/apyrimidinic endonuclease 1 ( APE 1), a dually functional protein possessing both base excision repair and redox activities, is involved in tumor angiogenesis, although these mechanisms are not fully understood. Our previous study showed that the expression of transforming growth factor β ( TGF β) was significantly reduced in  APE 1‐deficient osteosarcoma cells. Transforming growth factor β promotes cancer metastasis through various mechanisms including immunosuppression, angiogenesis, and invasion. In the current study, we initially revealed that  APE 1,  TGF β, and microvessel density ( MVD ) have pairwise correlation in osteosarcoma tissue samples, whereas  TGF β, tumor size, and  MVD  were inversely related to the prognosis of the cohort. We found that knocking down  APE 1 in osteosarcoma cells resulted in  TGF β downregulation. In addition,  APE 1‐si RNA  led to suppression of angiogenesis  in vitro  based on  HUVEC s in Transwell and Matrigel tube formation assays. Reduced secretory protein level of  TGF β of culture medium also resulted in decreased phosphorylation of Smad3 of  HUVEC s. In a mouse xenograft model, si RNA ‐mediated silencing of  APE 1 downregulated  TGF β expression, tumor size, and  MVD . Collectively, the current evidence indicates that  APE 1 regulates angiogenesis in osteosarcoma by controlling the  TGF β pathway, suggesting a novel target for anti‐angiogenesis therapy in human osteosarcoma.

Apurinic/apyrimidinic endonuclease 1 regulates angiogenesis in a transforming growth factor β‐dependent manner in human osteosarcoma