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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...

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Autores principales: Casciaro, Marco, Cardia, Roberta, Di Salvo, Eleonora, Tuccari, Giovanni, Ieni, Antonio, Gangemi, Sebastiano
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
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.
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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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