Hypoxia-induced ELF3 promotes tumor angiogenesis through IGF1/IGF1R

Seung Hee Seo, Soo Yeon Hwang, Seohui Hwang, Sunjung Han, Hyojin Park, Yun Sil Lee, Seung Bae Rho, Youngjoo Kwon

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13 Scopus citations


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.

Original languageEnglish
Article numbere52977
JournalEMBO Reports
Issue number8
StatePublished - 3 Aug 2022

Bibliographical note

Funding Information:
This work was supported by the Health Fellowship Foundation and the National Research Foundation of Korea (NRF) grant funded by the Korean government (MSIT) (2018R1A5A2025286) and by the Bio & Medical Technology Development Program of the NRF funded by MSIT (2021M3E5E7024855).

Publisher Copyright:
© 2022 The Authors. Published under the terms of the CC BY NC ND 4.0 license.


  • ELF3
  • hypoxia
  • insulin-like growth factor I
  • ovarian cancer
  • tumor angiogenesis


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