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Discontinuation of anti-VEGF cancer therapy promotes metastasis through a liver revascularization mechanism.

Abstract：

:The impact of discontinuation of anti-VEGF cancer therapy in promoting cancer metastasis is unknown. Here we show discontinuation of anti-VEGF treatment creates a time-window of profound structural changes of liver sinusoidal vasculatures, exhibiting hyper-permeability and enlarged open-pore sizes of the fenestrated endothelium and loss of VE-cadherin. The drug cessation caused highly leaky hepatic vasculatures permit tumour cell intravasation and extravasation. Discontinuation of an anti-VEGF antibody-based drug and sunitinib markedly promotes liver metastasis. Mechanistically, host hepatocyte, but not tumour cell-derived vascular endothelial growth factor (VEGF), is responsible for cancer metastasis. Deletion of hepatocyte VEGF markedly ablates the 'off-drug'-induced metastasis. These findings provide mechanistic insights on anti-VEGF cessation-induced metastasis and raise a new challenge for uninterrupted and sustained antiangiogenic therapy for treatment of human cancers.

journal_name

Nat Commun

journal_title

Nature communications

authors

Yang Y,Zhang Y,Iwamoto H,Hosaka K,Seki T,Andersson P,Lim S,Fischer C,Nakamura M,Abe M,Cao R,Skov PV,Chen F,Chen X,Lu Y,Nie G,Cao Y

doi

10.1038/ncomms12680

subject

Has Abstract

pub_date

2016-09-01 00:00:00

pages

12680

issn

2041-1723

pii

ncomms12680

journal_volume

7

pub_type

杂志文章

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