Background: Long non-coding RNAs (lncRNAs) X-inactive specific transcript (XIST) has identified to involve into the tumor cell angiogenesis. However, whether XIST contributes to Human Brain Microvascular Endothelial Cells (HBMEC) angiogenesis as well as potential mechanisms are largely unclear.
Methods: The expression of XIST, miR-485-3p and SRY-box 7 (SOX7) in HBMEC were altered by transfection. The cell viability, cell migration and tube formation of HBMEC were measured, respectively. The cross-regulations between XIST, miR-485-3p, SOX7, and vascular endothelial growth factor (VEGF) signaling pathway were investigated by RT-qPCR and Western blot assay.
Results: In this study, we characterized the upregulation of XIST in HBMEC under hypoxia condition. Meanwhile, XIST silencing impaired hypoxia-induced cell proliferation, migration and tube formation. Besides, our integrated experiments identified that XIST may competitively bind with miR-485-3p and then modulate the derepression of downstream target SRY-box 7 (SOX7). Mechanically, knockdown of XIST impaired hypoxia-induced angiogenesis via miR-485-3p/SOX7 axis and subsequent suppression of VEGF signaling pathway.
Conclusion: Altogether, the present study suggested that XIST is required to maintain VEGF signaling expression in HBMEC under hypoxia condition and plays a vital role in hypoxia-induced angiogenesis via miR-485-3p/SOX7 axis.
Keywords: Ischemic stroke; SOX7; XIST; angiogenesis; miR-485-3p.
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