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MINI REVIEW article

Front. Cell Dev. Biol.

Sec. Cancer Cell Biology

This article is part of the Research TopicAdvances in Gastrointestinal CancersView all 9 articles

Tumor suppressor function of Formyl Peptide Receptor 1 in gastrointestinal cancers: a focus on the underlying signaling

Provisionally accepted
Maria  MarottaMaria Marotta1Federica  LiottiFederica Liotti2Rosa Marina  MelilloRosa Marina Melillo2*Nella  PreveteNella Prevete3*
  • 1Istituto degli Endotipi in Oncologia Metabolismo e Immunologia G Salvatore, Naples, Italy
  • 2Universita degli Studi di Napoli Federico II, Naples, Italy
  • 3University of Naples Federico II, Naples, Italy

The final, formatted version of the article will be published soon.

The homeostasis of a tissue such the gastrointestinal (GI) tract is of fundamental importance for human health, given its constant exposure to a wide variety of external substances. The Formyl peptide Receptor 1 (FPR1) is an innate immune receptor belonging to the FPR family, that can recognize various endogenous danger-and exogenous pathogen-associated molecules, triggering inflammation. Importantly, depending on the context and on the specific ligand, FPR1 can also stimulate inflammation resolution. Thus, FPR1 is a critical actor in GI physiopathology. Interestingly, not only FPR1 participates and is necessary for maintaining homeostasis, but it also exerts strong tumor suppressor properties in this tissue. The present review discusses the mechanisms responsible for this specific function of FPR1 in cancer of the GI tract, focusing in particular on FPR1-mediated signal transduction.

Keywords: Formyl peptide receptor 1, Gastrointestinal epithelia, Cancer, tumor suppressor, signaling

Received: 27 Oct 2025; Accepted: 21 Nov 2025.

Copyright: © 2025 Marotta, Liotti, Melillo and Prevete. 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) or licensor 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.

* Correspondence:
Rosa Marina Melillo, rosmelil@unina.it
Nella Prevete, nella.prevete@unina.it

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