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首页> 外文期刊>Hypoxia >Induction of erythropoiesis by hypoxia-inducible factor prolyl hydroxylase inhibitors without promotion of tumor initiation, progression, or metastasis in a VEGF-sensitive model of spontaneous breast cancer
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Induction of erythropoiesis by hypoxia-inducible factor prolyl hydroxylase inhibitors without promotion of tumor initiation, progression, or metastasis in a VEGF-sensitive model of spontaneous breast cancer

机译：缺氧诱导因子脯氨酰羟化酶抑制剂诱导红细胞生成，而不会促进自发性乳腺癌的VEGF敏感性模型中的肿瘤发生，进展或转移

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The effects of pharmacological hypoxia-inducible factor (HIF) stabilization were investigated in the MMTV-Neundl-YD5 (NeuYD) mouse model of breast cancer. This study first confirmed the sensitivity of this model to increased vascular endothelial growth factor (VEGF), using bigenic NeuYD;MMTV-VEGF-25 mice. Tumor initiation was dramatically accelerated in bigenic animals. Bigenic tumors were also more aggressive, with shortened doubling times and increased lung metastasis as compared to NeuYD controls. In separate studies, NeuYD mice were treated three times weekly from 7 weeks of age until study end with two different HIF prolyl hydroxylase inhibitors (HIF-PHIs), FG-4497 or roxadustat (FG-4592). In NeuYD mice, HIF-PHI treatments elevated erythropoiesis markers, but no differences were detected in tumor onset or the phenotypes of established tumors.
机译：在乳腺癌的MMTV-Neu ndl -YD5（NeuYD）小鼠模型中研究了药理学缺氧诱导因子（HIF）稳定作用。这项研究首先使用双基因NeuYD; MMTV-VEGF-25小鼠证实了该模型对增加的血管内皮生长因子（VEGF）的敏感性。在双基因动物中，肿瘤的发生显着加速。与NeuYD对照相比，双基因肿瘤也更具侵略性，缩短了加倍时间并增加了肺转移。在单独的研究中，从7周龄开始，每周三次对NeuYD小鼠进行治疗，直到研究结束时用两种不同的HIF脯氨酰羟化酶抑制剂（HIF-PHIs），FG-4497或roxadustat（FG-4592）治疗。在NeuYD小鼠中，HIF-PHI治疗可提高红细胞生成指标，但在肿瘤发作或已建立肿瘤的表型中未发现差异。

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