Roles of IL-1 in Cancer: From Tumor Progression to Resistance to Targeted Therapies.
Animals
Clinical Trials as Topic
Drug Resistance, Neoplasm
/ drug effects
Humans
Immune Tolerance
/ immunology
Interleukin-1alpha
/ physiology
Interleukin-1beta
/ physiology
Ligands
Molecular Targeted Therapy
Neoplasms
/ blood supply
Neovascularization, Pathologic
/ metabolism
Receptors, Interleukin-1
/ antagonists & inhibitors
Tumor Microenvironment
IL-1
cancer
resistance
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
20 Aug 2020
20 Aug 2020
Historique:
received:
11
07
2020
revised:
04
08
2020
accepted:
18
08
2020
entrez:
23
8
2020
pubmed:
23
8
2020
medline:
14
4
2021
Statut:
epublish
Résumé
IL-1 belongs to a family of 11 members and is one of the seven receptor-agonists with pro-inflammatory activity. Beyond its biological role as a regulator of the innate immune response, IL-1 is involved in stress and chronic inflammation, therefore it is responsible for several pathological conditions. In particular, IL-1 is known to exert a critical function in malignancies, influencing the tumor microenvironment and promoting cancer initiation and progression. Thus, it orchestrates immunosuppression recruiting pro-tumor immune cells of myeloid origin. Furthermore, new recent findings showed that this cytokine can be directly produced by tumor cells in a positive feedback loop and contributes to the failure of targeted therapy. Activation of anti-apoptotic signaling pathways and senescence are some of the mechanisms recently proposed, but the role of IL-1 in tumor cells refractory to standard therapies needs to be further investigated.
Identifiants
pubmed: 32825489
pii: ijms21176009
doi: 10.3390/ijms21176009
pmc: PMC7503335
pii:
doi:
Substances chimiques
IL1A protein, human
0
IL1B protein, human
0
Interleukin-1alpha
0
Interleukin-1beta
0
Ligands
0
Receptors, Interleukin-1
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : PRIN2017
ID : 2017TATYMP_002
Organisme : ALAMIDEA
ID : ALMAIDEA2018
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