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Interleukin-33 Involvement in Nonsmall Cell Lung Carcinomas: An Update
Lung carcinogenesis is a multistep process involving genetic mutations and epigenetic changes, with the acquisition of a malignant phenotype characterized by apoptosis resistance, unregulated proliferation and differentiation, invasion, and metastatic abilities. However, neoplastic development and p...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6572046/ https://www.ncbi.nlm.nih.gov/pubmed/31130612 http://dx.doi.org/10.3390/biom9050203 |
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author | Casciaro, Marco Cardia, Roberta Di Salvo, Eleonora Tuccari, Giovanni Ieni, Antonio Gangemi, Sebastiano |
author_facet | Casciaro, Marco Cardia, Roberta Di Salvo, Eleonora Tuccari, Giovanni Ieni, Antonio Gangemi, Sebastiano |
author_sort | Casciaro, Marco |
collection | PubMed |
description | Lung carcinogenesis is a multistep process involving genetic mutations and epigenetic changes, with the acquisition of a malignant phenotype characterized by apoptosis resistance, unregulated proliferation and differentiation, invasion, and metastatic abilities. However, neoplastic development and progression seem to be aided by non-neoplastic cells; the molecules they produced can either promote the immune response or, alternatively, support tumor pathogenesis. Consequently, the relative contribution of tumor-associated inflammatory pathways to cancer development has become crucial information. Interleukin-33 (IL-33) is an IL-1-like alarmin, and it is a ligand for the suppressor of tumorigenicity 2 (ST2) receptor. IL-33 functions as a dual role cytokine with the ability to induce T-helper-type 2 (Th2) immune cells and translocate into the nucleus, suppressing gene transcription. Although its function in immunity- and immune-related disorders is well known, its role in tumorigenesis is still debated. The IL-33/ST2 axis is emerging as a powerful modulator of the tumor microenvironment (TME) by recruiting immune cells, able to modify the TME, supporting malignant proliferation or improving antitumor immunity. In the present review, we discuss IL-33′s potential role in lung carcinogenesis and its possible application as a therapeutic target. |
format | Online Article Text |
id | pubmed-6572046 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-65720462019-06-18 Interleukin-33 Involvement in Nonsmall Cell Lung Carcinomas: An Update Casciaro, Marco Cardia, Roberta Di Salvo, Eleonora Tuccari, Giovanni Ieni, Antonio Gangemi, Sebastiano Biomolecules Review Lung carcinogenesis is a multistep process involving genetic mutations and epigenetic changes, with the acquisition of a malignant phenotype characterized by apoptosis resistance, unregulated proliferation and differentiation, invasion, and metastatic abilities. However, neoplastic development and progression seem to be aided by non-neoplastic cells; the molecules they produced can either promote the immune response or, alternatively, support tumor pathogenesis. Consequently, the relative contribution of tumor-associated inflammatory pathways to cancer development has become crucial information. Interleukin-33 (IL-33) is an IL-1-like alarmin, and it is a ligand for the suppressor of tumorigenicity 2 (ST2) receptor. IL-33 functions as a dual role cytokine with the ability to induce T-helper-type 2 (Th2) immune cells and translocate into the nucleus, suppressing gene transcription. Although its function in immunity- and immune-related disorders is well known, its role in tumorigenesis is still debated. The IL-33/ST2 axis is emerging as a powerful modulator of the tumor microenvironment (TME) by recruiting immune cells, able to modify the TME, supporting malignant proliferation or improving antitumor immunity. In the present review, we discuss IL-33′s potential role in lung carcinogenesis and its possible application as a therapeutic target. MDPI 2019-05-25 /pmc/articles/PMC6572046/ /pubmed/31130612 http://dx.doi.org/10.3390/biom9050203 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Casciaro, Marco Cardia, Roberta Di Salvo, Eleonora Tuccari, Giovanni Ieni, Antonio Gangemi, Sebastiano Interleukin-33 Involvement in Nonsmall Cell Lung Carcinomas: An Update |
title | Interleukin-33 Involvement in Nonsmall Cell Lung Carcinomas: An Update |
title_full | Interleukin-33 Involvement in Nonsmall Cell Lung Carcinomas: An Update |
title_fullStr | Interleukin-33 Involvement in Nonsmall Cell Lung Carcinomas: An Update |
title_full_unstemmed | Interleukin-33 Involvement in Nonsmall Cell Lung Carcinomas: An Update |
title_short | Interleukin-33 Involvement in Nonsmall Cell Lung Carcinomas: An Update |
title_sort | interleukin-33 involvement in nonsmall cell lung carcinomas: an update |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6572046/ https://www.ncbi.nlm.nih.gov/pubmed/31130612 http://dx.doi.org/10.3390/biom9050203 |
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