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肿瘤坏死因子-α通过诱导血管内皮生长因子促进肿瘤生长。

Tumor necrosis factor-alpha promotes tumor growth by inducing vascular endothelial growth factor.

机构信息

Tumor Immunology and Gene Therapy Center, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai, China.

出版信息

Cancer Invest. 2011 Aug;29(7):485-93. doi: 10.3109/07357907.2011.597812.

DOI:10.3109/07357907.2011.597812
PMID:21740086
Abstract

Tumor necrosis factor (TNF)-α has been proved as an adjuvant therapy for tumor by FDA. However, the effect of chronic TNF-α expression for tumor is still controversial. In this study, we investigated the effect of low-dose TNF-α on tumor growth. We confirmed that low-dose TNF-α promoted angiogenesis of tumor in vivo, vascular endothelial growth factor (VEGF) and hypoxia-inducible factor (HIF)-1α, the transcription factor of VEGF, were both upregulated. Our results suggested that low-dose TNF-α was a powerful activator of angiogenesis in tumor and HIF-1α-VEGF pathway seemed to be the most important molecular mechanism.

摘要

肿瘤坏死因子 (TNF)-α 已被 FDA 证实为肿瘤的辅助治疗药物。然而,慢性 TNF-α 表达对肿瘤的影响仍存在争议。在本研究中,我们研究了低剂量 TNF-α 对肿瘤生长的影响。我们证实低剂量 TNF-α促进了体内肿瘤的血管生成,血管内皮生长因子 (VEGF) 和缺氧诱导因子 (HIF)-1α,即 VEGF 的转录因子,均上调。我们的结果表明,低剂量 TNF-α是肿瘤血管生成的有力激活剂,HIF-1α-VEGF 途径似乎是最重要的分子机制。

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