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. 2022 Dec 5;13:1078766. doi: 10.3389/fphar.2022.1078766

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Copyright © 2022 Lai, Liu, Wu, Cai, Jie, Xu and Deng.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Tumor-promoting inflammation-related signals that can be targeted by NSAIDs. Both infectious and non-infectious chronic inflammation contributes to carcinogenesis via increasing PGs and activating COX-independent signals that can be suppressed by NSAIDs. These COX-dependent and independent pathways promote cancer development by inducing resistance to PCD, and facilitating proliferation, migration and invasion. Induction of tumor angiogenesis, immunosuppressive TME and other mechanisms are also achieved by NSAID-targeted signals. Abbreviations: HBV, hepatitis B virus; IBD, inflammatory bowel disease; PGs, prostaglandins; PCD, programmed cell death; TME, tumor microenvironment.