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. 2022 Aug 19;13(8):724. doi: 10.1038/s41419-022-05171-3

Fig. 8. Schematic diagram of FGF-2-FGFR1-ERK-MYC axis mediates AAD resistance and metastasis in NPC.

Fig. 8

NPC cancer cells often produce FGF-2, and FGF-2 impedes the AAD-mediated anti-EC effect in the TME. In FGF-2 positive tumors, the FGFR1-ERK-MYC axis is upregulated in ECs and compensates for VEGF-VEGFR2-MYC signaling. MYC further drives downstream angiogenic genes, hence keep the angiogenesis in the TME. Angiogenic tumor vessels further facilitate tumor cell intravasation and pulmonary metastasis. In such FGF-2 high TME, inhibition of VEGF-VEGFR2 signaling alone does not effectively inhibit angiogenesis. Lenvatinib, an FDA-approved multi-kinase inhibitor targeting both VEGFR2 and FGFR1, exhibits robust antiangiogenic and anti-tumor effects in NPC or possibly FGF-2-rich tumors.