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. 2019 Dec 18;21(1):10. doi: 10.3390/ijms21010010

Figure 2.

Figure 2

The MKIs (sunitinib, sorafenib, lenvatinib, pazopanib, cabozantinib, and vandetanib) block signaling from the tyrosine kinase receptors, thus preventing phosphorylation and, ultimately, angiogenesis and tumor growth. Furthermore, the interplay between the tumor cells, endothelial cells, and pericytes are shown by the downregulation of the tumor suppressor, VHL, and thereby less inhibition of HIF, which causes an increased induction of angiogenesis due to the production of VEGF and PDGF (green arrows) [11,24,26,29]. Abbreviations: RAS (rat sarcoma protein), RAF (rapidly accelerated fibrosarcoma kinase), MEK (mitogen-activated protein kinase kinase), ERK (mitogen-activated protein kinase), PI3K (phosphoinositide 3-kinase), AKT (protein kinase B), mTOR (mammalian target of rapamycin), VHL (von Hippel–Lindau tumor suppressor), HIF (hypoxia-inducible factor). Crossed-out arrows represent the inhibited signaling pathways by the indicated drugs.