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. 2021 Dec 17;71(9):1843–1855. doi: 10.1136/gutjnl-2021-325180

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© Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

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Schematic showing the mechanism by which tumour stroma-targeted TRAIL-NO@Nanogel suppresses PDAC progression in mice. NO released from tumour stroma-targeted TRAIL-NO@Nanogel remodels the fibrotic tumour microenvironment of desmoplastic PDAC. (1) NO released from NPs modified with tumour stroma-targeting peptides identified by phage display suppresses PSC activation, reduces ECM production and increases tumour perfusion in PDAC. (2) NO reprogrammes the desmoplastic stroma and overcomes TRAIL resistance, sensitising PDAC tumours to TRAIL therapy. (3) Co-delivery of TRAIL and NO by tumour stroma-targeted TRAIL-NO@Nanogel efficiently suppresses tumour growth. ECM, extracellular matrix; NO, nitric oxide; NPs, nanoparticle; PDAC, pancreatic ductal adenocarcinoma; PSC, pancreatic stellate cells; TRAIL, tumour necrosis factor-related apoptosis-inducing ligand.