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However, GSH-deficient FoB accumulate defective mitochondria and do not activate upon viral challenge

In hypoxic epithelial ovarian cancer, as a transcription factor of IGF-1, highly expressed ELF3-mediated secretion of IGF-1 and VEGF promoted endothelial cell proliferation, migration and tumor angiogenesis through activation of the tyrosine kinase pathway, whereas ELF3 silencing attenuated angiogenesis and tumorigenesis in a xenograft mouse model, demonstrating the pro-vascular effect of IGF-1 (39)

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