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Therapeutic paradigm of dual targeting VEGF and PDGF for effectively treating FGF-2 off-target tumors

by Sun, Xiaoting , Hosaka, Kayoko , Zhang, Yin , Li, Qi , Liu, Xialin , He, Xingkang , Wu, Jieyu , Li, Xuri , Yang, Yunlong , Nakamura, Masaki , Liu, Yizhi , Jing, Xu , Cao, Yihai , Seki, Takahiro , Xu, Yuanfu , Scherzer, Martin , Chen, Yuguo , Du, Qiqiao , Morikawa, Hiromasa , Hong, An , Cheng, Tao

in 631/67/1059/2326 / 631/67/1857 / 631/67/2328 / Ablation / Angiogenesis / Antiangiogenic agents / Antiangiogenics / Anticancer properties / Antitumor activity / Biomarkers / Blood vessels / Breast cancer / Drug delivery / Fibroblast growth factor 2 / Fibrosarcoma / Humanities and Social Sciences / multidisciplinary / Optimization / Pericytes / Platelet-derived growth factor / Science / Science (multidisciplinary) / Tumors / Vascular endothelial growth factor / Vascularization

2020

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2020

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2020

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Journal Article

Therapeutic paradigm of dual targeting VEGF and PDGF for effectively treating FGF-2 off-target tumors

Sun, Xiaoting,

Hosaka, Kayoko,

Zhang, Yin,

Li, Qi,

Liu, Xialin,

He, Xingkang,

Wu, Jieyu,

Li, Xuri,

Yang, Yunlong,

Nakamura, Masaki,

Liu, Yizhi,

Jing, Xu,

Cao, Yihai,

Seki, Takahiro,

Xu, Yuanfu,

Scherzer, Martin,

Chen, Yuguo,

Du, Qiqiao,

Morikawa, Hiromasa,

Hong, An,

Cheng, Tao

2020

Overview

FGF-2 displays multifarious functions in regulation of angiogenesis and vascular remodeling. However, effective drugs for treating FGF-2 + tumors are unavailable. Here we show that FGF-2 modulates tumor vessels by recruiting NG2 + pricytes onto tumor microvessels through a PDGFRβ-dependent mechanism. FGF-2 + tumors are intrinsically resistant to clinically available drugs targeting VEGF and PDGF. Surprisingly, dual targeting the VEGF and PDGF signaling produces a superior antitumor effect in FGF-2 + breast cancer and fibrosarcoma models. Mechanistically, inhibition of PDGFRβ ablates FGF-2-recruited perivascular coverage, exposing anti-VEGF agents to inhibit vascular sprouting. These findings show that the off-target FGF-2 is a resistant biomarker for anti-VEGF and anti-PDGF monotherapy, but a highly beneficial marker for combination therapy. Our data shed light on mechanistic interactions between various angiogenic and remodeling factors in tumor neovascularization. Optimization of antiangiogenic drugs with different principles could produce therapeutic benefits for treating their resistant off-target cancers. Anti-VEGF therapy has many limitations that might be resolved by using combination treatment approaches. Here, the authors demonstrate that the dual-targeting of VEGF and PDGF is required for targeting resistant FGF2+ tumors which depend on the recruitment of pericytes on tumor microvessels.

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Publisher

Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio

Subject

/ Antiangiogenic agents

/ Antiangiogenics