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The aim of this study was to determine hown–3 polyunsaturated fatty acid (PUFAs) counteracted tumor chemoresistance by restoring a functional vascularization. Rats with chemically induced mammary tumors were divided into two nutritional groups: a control group and a group fed with ann–3 PUFA-enriched diet. Both groups were treated with docetaxel. Functional vascular parameters (ultrasounds, interstitial fluid pressure) were determined for both nutritional groups before (W0) and during docetaxel treatment [every 2 h up to 1 week (W+1) for interstitial fluid pressure, at W+1for Evans blue extravasation and at W+2and W+6for ultrasounds].In vitro  n–3 PUFA-induced changes in endothelial cell migration, permeability and phosphorylation of endothelial nitric oxide synthase were evaluated using human umbilical vein endothelial cells. Whereas docetaxel stabilized tumor growth in the rat control group, it induced a 50% tumor regression in then–3 PUFA group. Ultrasounds parameters were consistently lower in then–3 PUFA group at all time points measured, down to ∼50% at W+6. A single dose of docetaxel in then–3 PUFA group markedly reduced interstitial fluid pressure from 2 h after injection up to W+1when Evans blue extravasation was increased by 3-fold. A decreased activation of endothelial nitric oxide synthase in tumors of then–3 PUFA group, and in human umbilical vein endothelial cell cultured withn–3 PUFA, points toward a PUFA-induced disruption of nitric oxide signaling pathway. This normalization of tumor vasculature functions undern–3 PUFA diet indicates that such a supplementation, by improving drug delivery in mammary tumors, could be a complementary clinical strategy to decrease anticancer drug resistance.

Reducing endothelial NOS activation and interstitial fluid pressure with n –3 PUFA offset tumor chemoresistance