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Minocycline accelerates hypoxia-inducible factor-1 alpha degradation and inhibits hypoxia-induced neovasculogenesis through prolyl hydroxylase, von Hippel–Lindau-dependent pathway
Minocycline speeds up breakdown of a low-oxygen response protein and blocks new blood vessel growth caused by low oxygen through a specific cell pathway
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Abstract
Minocycline induces HIF-1α proteasomal degradation under hypoxia in lung adenocarcinoma cell lines.
- Exposure to minocycline increases the expression of prolyl hydroxylase-2, enhancing the degradation of HIF-1α.
- Minocycline promotes the interaction between HIF-1α and the von Hippel-Lindau protein, contributing to HIF-1α degradation.
- The degradation of HIF-1α by minocycline occurs independently of pathways involving phosphatidylinositol-3 kinase/Akt/mTOR or Hsp90.
- Hypoxia-conditioned cells pretreated with minocycline demonstrate reduced expression of hypoxia response element reporters.
- Minocycline treatment leads to decreased expression of vascular endothelial growth factor C/D, matrix metalloproteinase 2, and glucose transporter 1.
- By reducing VEGF secretion in cancerous cells, minocycline may inhibit neovasculogenesis in endothelial cells.
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