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Retinoic acid induces hypersegmentation and enhances cytotoxicity of neutrophils against cancer cells.

Abstract
Hypersegmentation of nuclei is considered a distinct characteristic of the antitumoral phenotype of neutrophils. Retinoic acid, a metabolite of retinol, reorganizes and induces segmentation of the nucleus during the differentiation of neutrophils. However, the role of retinoic acid in the phenotype polarization of neutrophils has not been fully established. Here, we investigated the effect of retinoic acid on phenotype polarization of neutrophils. Retinoic acid-induced the hypersegmentation of human neutrophils via retinoic acid receptors and mTOR pathways. Retinoic acid-induced hypersegmented neutrophils enhanced neutrophil extracellular traps (NETs) formation in response to phorbol-12-myristate 13-acetate (PMA) and fMLP (N-Formylmethionine-leucyl-phenylalanine) stimulation, and increased cytotoxicity against various tumor cells. Moreover, retinoic acid treatment attenuated tumor growth in a murine model of tumor. Taken together, these results suggests that retinoic acid induces the phenotype polarization of neutrophils to exert antitumor effects.
AuthorsSanjeeb Shrestha, Shin-Yeong Kim, Young-Jin Yun, Jun-Kyu Kim, Jae Man Lee, Minsang Shin, Dong-Keun Song, Chang-Won Hong
JournalImmunology letters (Immunol Lett) Vol. 182 Pg. 24-29 (02 2017) ISSN: 1879-0542 [Electronic] Netherlands
PMID28065603 (Publication Type: Journal Article)
CopyrightCopyright © 2017 European Federation of Immunological Societies. Published by Elsevier B.V. All rights reserved.
Chemical References
  • Reactive Oxygen Species
  • Receptors, Retinoic Acid
  • Tretinoin
  • TOR Serine-Threonine Kinases
Topics
  • Animals
  • Cytotoxicity, Immunologic (drug effects)
  • Extracellular Traps (drug effects, immunology)
  • Female
  • Humans
  • Leukocyte Disorders (chemically induced, immunology, metabolism)
  • Mice
  • Neoplasms (immunology, metabolism, pathology)
  • Neutrophils (drug effects, immunology, metabolism, pathology)
  • Reactive Oxygen Species
  • Receptors, Retinoic Acid (metabolism)
  • TOR Serine-Threonine Kinases (metabolism)
  • Tretinoin (pharmacology)
  • Tumor Microenvironment (drug effects, genetics)

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