Molecular Mechanisms and Cellular Contribution from Lung Fibrosis to Lung Cancer Development

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, fibrosing interstitial lung disease (ILD) of unknown aetiology, with a median survival of 2–4 years from the time of diagnosis. Although IPF has unknown aetiology by definition, there have been identified several risks factors increasing...

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Autores principales:	Anna Valeria Samarelli, Valentina Masciale, Beatrice Aramini, Georgina Pamela Coló, Roberto Tonelli, Alessandro Marchioni, Giulia Bruzzi, Filippo Gozzi, Dario Andrisani, Ivana Castaniere, Linda Manicardi, Antonio Moretti, Luca Tabbì, Giorgia Guaitoli, Stefania Cerri, Massimo Dominici, Enrico Clini
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	idiopathic pulmonary fibrosis lung cancer myofibroblast cancer associated fibroblasts (CAFs) mechanotrasduction Biology (General) QH301-705.5 Chemistry QD1-999
Acceso en línea:	https://doaj.org/article/de2bff62966847629554c5c69aa0c5db
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spelling	oai:doaj.org-article:de2bff62966847629554c5c69aa0c5db2021-11-25T17:54:02ZMolecular Mechanisms and Cellular Contribution from Lung Fibrosis to Lung Cancer Development10.3390/ijms2222121791422-00671661-6596https://doaj.org/article/de2bff62966847629554c5c69aa0c5db2021-11-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/22/12179https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, fibrosing interstitial lung disease (ILD) of unknown aetiology, with a median survival of 2–4 years from the time of diagnosis. Although IPF has unknown aetiology by definition, there have been identified several risks factors increasing the probability of the onset and progression of the disease in IPF patients such as cigarette smoking and environmental risk factors associated with domestic and occupational exposure. Among them, cigarette smoking together with concomitant emphysema might predispose IPF patients to lung cancer (LC), mostly to non-small cell lung cancer (NSCLC), increasing the risk of lung cancer development. To this purpose, IPF and LC share several cellular and molecular processes driving the progression of both pathologies such as fibroblast transition proliferation and activation, endoplasmic reticulum stress, oxidative stress, and many genetic and epigenetic markers that predispose IPF patients to LC development. Nintedanib, a tyrosine–kinase inhibitor, was firstly developed as an anticancer drug and then recognized as an anti-fibrotic agent based on the common target molecular pathway. In this review our aim is to describe the updated studies on common cellular and molecular mechanisms between IPF and lung cancer, knowledge of which might help to find novel therapeutic targets for this disease combination.Anna Valeria SamarelliValentina MascialeBeatrice AraminiGeorgina Pamela ColóRoberto TonelliAlessandro MarchioniGiulia BruzziFilippo GozziDario AndrisaniIvana CastaniereLinda ManicardiAntonio MorettiLuca TabbìGiorgia GuaitoliStefania CerriMassimo DominiciEnrico CliniMDPI AGarticleidiopathic pulmonary fibrosislung cancermyofibroblastcancer associated fibroblasts (CAFs)mechanotrasductionBiology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 12179, p 12179 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	idiopathic pulmonary fibrosis lung cancer myofibroblast cancer associated fibroblasts (CAFs) mechanotrasduction Biology (General) QH301-705.5 Chemistry QD1-999
spellingShingle	idiopathic pulmonary fibrosis lung cancer myofibroblast cancer associated fibroblasts (CAFs) mechanotrasduction Biology (General) QH301-705.5 Chemistry QD1-999 Anna Valeria Samarelli Valentina Masciale Beatrice Aramini Georgina Pamela Coló Roberto Tonelli Alessandro Marchioni Giulia Bruzzi Filippo Gozzi Dario Andrisani Ivana Castaniere Linda Manicardi Antonio Moretti Luca Tabbì Giorgia Guaitoli Stefania Cerri Massimo Dominici Enrico Clini Molecular Mechanisms and Cellular Contribution from Lung Fibrosis to Lung Cancer Development
description	Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, fibrosing interstitial lung disease (ILD) of unknown aetiology, with a median survival of 2–4 years from the time of diagnosis. Although IPF has unknown aetiology by definition, there have been identified several risks factors increasing the probability of the onset and progression of the disease in IPF patients such as cigarette smoking and environmental risk factors associated with domestic and occupational exposure. Among them, cigarette smoking together with concomitant emphysema might predispose IPF patients to lung cancer (LC), mostly to non-small cell lung cancer (NSCLC), increasing the risk of lung cancer development. To this purpose, IPF and LC share several cellular and molecular processes driving the progression of both pathologies such as fibroblast transition proliferation and activation, endoplasmic reticulum stress, oxidative stress, and many genetic and epigenetic markers that predispose IPF patients to LC development. Nintedanib, a tyrosine–kinase inhibitor, was firstly developed as an anticancer drug and then recognized as an anti-fibrotic agent based on the common target molecular pathway. In this review our aim is to describe the updated studies on common cellular and molecular mechanisms between IPF and lung cancer, knowledge of which might help to find novel therapeutic targets for this disease combination.
format	article
author	Anna Valeria Samarelli Valentina Masciale Beatrice Aramini Georgina Pamela Coló Roberto Tonelli Alessandro Marchioni Giulia Bruzzi Filippo Gozzi Dario Andrisani Ivana Castaniere Linda Manicardi Antonio Moretti Luca Tabbì Giorgia Guaitoli Stefania Cerri Massimo Dominici Enrico Clini
author_facet	Anna Valeria Samarelli Valentina Masciale Beatrice Aramini Georgina Pamela Coló Roberto Tonelli Alessandro Marchioni Giulia Bruzzi Filippo Gozzi Dario Andrisani Ivana Castaniere Linda Manicardi Antonio Moretti Luca Tabbì Giorgia Guaitoli Stefania Cerri Massimo Dominici Enrico Clini
author_sort	Anna Valeria Samarelli
title	Molecular Mechanisms and Cellular Contribution from Lung Fibrosis to Lung Cancer Development
title_short	Molecular Mechanisms and Cellular Contribution from Lung Fibrosis to Lung Cancer Development
title_full	Molecular Mechanisms and Cellular Contribution from Lung Fibrosis to Lung Cancer Development
title_fullStr	Molecular Mechanisms and Cellular Contribution from Lung Fibrosis to Lung Cancer Development
title_full_unstemmed	Molecular Mechanisms and Cellular Contribution from Lung Fibrosis to Lung Cancer Development
title_sort	molecular mechanisms and cellular contribution from lung fibrosis to lung cancer development
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/de2bff62966847629554c5c69aa0c5db
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Molecular Mechanisms and Cellular Contribution from Lung Fibrosis to Lung Cancer Development

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