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低氧诱导的 ELF3 通过 IGF1/IGF1R 促进肿瘤血管生成。

Hypoxia-induced ELF3 promotes tumor angiogenesis through IGF1/IGF1R.

机构信息

College of Pharmacy, Graduate School of Pharmaceutical Sciences, Ewha Womans University, Seoul, Korea.

Research Institute, National Cancer Center, Goyang-si Gyeonggi-do, Korea.

出版信息

EMBO Rep. 2022 Aug 3;23(8):e52977. doi: 10.15252/embr.202152977. Epub 2022 Jun 13.

DOI:10.15252/embr.202152977
PMID:35695065
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9346469/
Abstract

Epithelial ovarian cancer (EOC) is one of the most lethal gynecological cancers despite a relatively low incidence. Angiogenesis, one of the hallmarks of cancer, is essential for the pathogenesis of EOC, which is related to the induction of angiogenic factors. We found that ELF3 was highly expressed in EOCs under hypoxia and functioned as a transcription factor for IGF1. The ELF3-mediated increase in the secretion of IGF1 and VEGF promoted endothelial cell proliferation, migration, and EOC angiogenesis. Although this situation was much exaggerated under hypoxia, ELF3 silencing under hypoxia significantly attenuated angiogenic activity in endothelial cells by reducing the expression and secretion of IGF1 and VEGF. ELF3 silencing attenuated angiogenesis and tumorigenesis in ex vivo and xenograft mouse models. Consequently, ELF3 plays an important role in the induction of angiogenesis and tumorigenesis in EOC as a transcription factor of IGF1. A detailed understanding of the biological mechanism of ELF3 may both improve current antiangiogenic therapies and have anticancer effects for EOC.

摘要

上皮性卵巢癌 (EOC) 尽管发病率相对较低，但仍是最致命的妇科癌症之一。血管生成是癌症的标志之一，对于 EOC 的发病机制至关重要，这与血管生成因子的诱导有关。我们发现，ELF3 在缺氧条件下在上皮性卵巢癌细胞中高表达，并作为 IGF1 的转录因子发挥作用。ELF3 介导的 IGF1 和 VEGF 分泌增加促进了内皮细胞的增殖、迁移和 EOC 血管生成。尽管在缺氧条件下这种情况被大大夸大了，但缺氧条件下 ELF3 的沉默通过降低 IGF1 和 VEGF 的表达和分泌，显著减弱了内皮细胞的血管生成活性。ELF3 沉默减弱了体外和异种移植小鼠模型中的血管生成和肿瘤发生。因此，ELF3 作为 IGF1 的转录因子，在上皮性卵巢癌中诱导血管生成和肿瘤发生中发挥重要作用。详细了解 ELF3 的生物学机制可能既可以改善当前的抗血管生成治疗，又可以对 EOC 产生抗癌作用。

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