Added by | Nathalie Bonnefoy |
---|---|
Group name | EquipeNB |
Item Type | Journal Article |
Title | The Emerging Role of the IL-17B/IL-17RB Pathway in Cancer |
Creator | Bastid et al. |
Author | Jérémy Bastid |
Author | Cécile Dejou |
Author | Aurélie Docquier |
Author | Nathalie Bonnefoy |
Abstract | Among inflammatory mediators, a growing body of evidence emphasizes the contribution of the interleukin 17 (IL-17) cytokine family in malignant diseases. Besides IL-17A, the prototypic member of the IL-17 family, several experimental findings strongly support the role of the IL-17B/IL-17 receptor B (IL-17RB) pathway in tumorigenesis and resistance to anticancer therapies. In mouse models, IL-17B signaling through IL-17RB directly promotes cancer cell survival, proliferation, and migration, and induces resistance to conventional chemotherapeutic agents. Importantly, recent work by our and other laboratories showed that IL-17B signaling dramatically alters the tumor microenvironment by promoting chemokine and cytokine secretion which foster tumor progression. Moreover, the finding that elevated IL-17B is associated with poor prognosis in patients with pancreatic, gastric, lung, and breast cancer strengthens the results obtained in pre-clinical studies and highlights its clinical relevance. Here, we review the current understanding on the IL-17B/IL-17RB expression patterns and biological activities in cancer and highlight issues that remain to be addressed to better characterize IL-17B and its receptor as potential targets for enhancing the effectiveness of the existing cancer therapies. |
Publication | Frontiers in Immunology |
Volume | 11 |
Pages | 718 |
Date | 2020 |
Journal Abbr | Front Immunol |
Language | eng |
DOI | 10.3389/fimmu.2020.00718 |
ISSN | 1664-3224 |
Library Catalog | PubMed |
Extra | PMID: 32373132 PMCID: PMC7186465 |
Tags | cancer, cancer therapy, first-last-corresponding, IL-17, IL-17B, IL-17RB, review |
Date Added | 2020/07/29 - 15:05:55 |
Date Modified | 2020/07/29 - 15:26:55 |
Notes and Attachments | PubMed entry (Attachment) Texte intégral (Attachment) |