Figure 1.

Molecular signals orchestrated by HSP90-stabilized and hypoxia-activated PRKD2 during tumor growth and angiogenesis. Stabilization of PRKD2 by HSP90 contributes to enhanced tumor viability and vascularization. In this scenario, PRKD2 is responsible for augmented HIF-1α accumulation in a low-oxygen environment, resulting in activation of NF-κB and its target VEGFA. The extent to which PRKD2 regulates VEGFA secretion, either directly through HIF-1α and/or TR3/Nur77 or indirectly through NF-κB, remains to be elucidated. PRKD2, protein kinase D2; HSP90, heat shock protein 90; HIF-1α, hypoxia-inducible factor 1-α; VEGFA, vascular endothelial growth factor A. ? unknown molecule.