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Targeting the Canonical WNT/β-Catenin Pathway in Cancer Treatment Using Non-Steroidal Anti-Inflammatory Drugs

1
Diagnosis and Therapeutic Center, Hypertension and Cardiovascular Prevention Unit, Hotel-Dieu Hospital, AP-HP, Université Paris Descartes, 75004 Paris, France
2
Centre de Recherche Clinique, Grand Hôpital de l’Est Francilien (GHEF), 6–8 rue Saint-fiacre, 77100 Meaux, France
3
Centre Hospitalier Universitaire (CHU) Amiens Picardie, Université Picardie Jules Verne (UPJV), 80054 Amiens, France
4
Laboratoire de Mathématiques et Applications (LMA), UMR CNRS 7348, Université de Poitiers, 86000 Poitiers, France
*
Author to whom correspondence should be addressed.
Cells 2019, 8(7), 726; https://doi.org/10.3390/cells8070726
Received: 2 May 2019 / Revised: 11 July 2019 / Accepted: 14 July 2019 / Published: 15 July 2019
(This article belongs to the Special Issue Wnt Signaling in Health and Diseases)
Chronic inflammation and oxidative stress are common and co-substantial pathological processes accompanying and contributing to cancers. Numerous epidemiological studies have indicated that non-steroidal anti-inflammatory drugs (NSAIDs) could have a positive effect on both the prevention of cancer and tumor therapy. Numerous hypotheses have postulated that NSAIDs could slow tumor growth by acting on both chronic inflammation and oxidative stress. This review takes a closer look at these hypotheses. In the cancer process, one of the major signaling pathways involved is the WNT/β-catenin pathway, which appears to be upregulated. This pathway is closely associated with both chronic inflammation and oxidative stress in cancers. The administration of NSAIDs has been observed to help in the downregulation of the WNT/β-catenin pathway and thus in the control of tumor growth. NSAIDs act as PPARγ agonists. The WNT/β-catenin pathway and PPARγ act in opposing manners. PPARγ agonists can promote cell cycle arrest, cell differentiation, and apoptosis, and can reduce inflammation, oxidative stress, proliferation, invasion, and cell migration. In parallel, the dysregulation of circadian rhythms (CRs) contributes to cancer development through the upregulation of the canonical WNT/β-catenin pathway. By stimulating PPARγ expression, NSAIDs can control CRs through the regulation of many key circadian genes. The administration of NSAIDs in cancer treatment would thus appear to be an interesting therapeutic strategy, which acts through their role in regulating WNT/β-catenin pathway and PPARγ activity levels. View Full-Text
Keywords: non-steroidal anti-inflammatory drug; cancer; WNT; inflammation; oxidative stress; PPARγ non-steroidal anti-inflammatory drug; cancer; WNT; inflammation; oxidative stress; PPARγ
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Vallée, A.; Lecarpentier, Y.; Vallée, J.-N. Targeting the Canonical WNT/β-Catenin Pathway in Cancer Treatment Using Non-Steroidal Anti-Inflammatory Drugs. Cells 2019, 8, 726.

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