Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, CB2 3EG, UK.
Int J Hematol. 2012 May;95(5):471-7. doi: 10.1007/s12185-012-1072-3. Epub 2012 May 8.
Tumour growth at primary or secondary extravasation sites leads to localised regions of reduced oxygen tension (hypoxia) in cells both within and surrounding the tumour. Although the angiogenic response of the tumour cell to hypoxia has been widely examined, the effect of hypoxia on other cell types within the tumour microenvironment is less clear. The endothelium is highly responsive to local hypoxia and regulates tumour cell dissemination and ultimately metastatic success through differential regulation of hypoxia-inducible transcription factors (HIFs). The endothelial response to hypoxia particularly mediates key processes that regulate tumour vascularisation and cancer progression, including proliferation, migration, adherence, and vascular permeability. This article describes current understanding of the HIF-mediated endothelial response to hypoxia during cancer progression. Endothelial HIF signalling regulates tumour growth and metastasis and is therefore an attractive putative target for treatments that inhibit cancer progression.
原发性或继发性渗出部位的肿瘤生长导致肿瘤内和周围细胞中的局部氧张力（缺氧）降低。尽管肿瘤细胞对缺氧的血管生成反应已被广泛研究，但缺氧对肿瘤微环境中其他细胞类型的影响尚不明确。内皮细胞对局部缺氧高度敏感，并通过差异调节缺氧诱导转录因子（HIFs）来调节肿瘤细胞的扩散，最终影响转移的成功。内皮对缺氧的反应特别介导了调节肿瘤血管生成和癌症进展的关键过程，包括增殖、迁移、黏附和血管通透性。本文描述了目前对癌症进展过程中 HIF 介导的内皮对缺氧反应的理解。内皮细胞 HIF 信号转导调节肿瘤生长和转移，因此是抑制癌症进展的潜在治疗靶点。
