Molecular mechanisms and cellular contribution from lung fibrosis to lung cancer development

Autores
Samarelli, Anna Valeria; Masciale, Valentina; Aramini, Beatrice; Colo, Georgina Pamela; Tonelli, Roberto; Marchioni, Alessandro; Bruzzi, Giulia; Gozzi, Filippo; Andrisani, Dario; Castaniere, Ivana; Manicardi, Linda; Moretti, Antonio; Tabbì, Luca; Guaitoli, Giorgia; Cerri, Stefania; Dominici, Massimo; Clini, Enrico
Año de publicación
2021
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
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.
Fil: Samarelli, Anna Valeria. Università di Modena e Reggio Emilia; Italia
Fil: Masciale, Valentina. Università di Modena e Reggio Emilia; Italia
Fil: Aramini, Beatrice. Università di Modena e Reggio Emilia; Italia. Universidad de Bologna; Italia
Fil: Colo, Georgina Pamela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina
Fil: Tonelli, Roberto. Università di Modena e Reggio Emilia; Italia
Fil: Marchioni, Alessandro. Università di Modena e Reggio Emilia; Italia
Fil: Bruzzi, Giulia. Università di Modena e Reggio Emilia; Italia
Fil: Gozzi, Filippo. Università di Modena e Reggio Emilia; Italia
Fil: Andrisani, Dario. Università di Modena e Reggio Emilia; Italia
Fil: Castaniere, Ivana. Università di Modena e Reggio Emilia; Italia
Fil: Manicardi, Linda. Università di Modena e Reggio Emilia; Italia
Fil: Moretti, Antonio. Università di Modena e Reggio Emilia; Italia
Fil: Tabbì, Luca. Università di Modena e Reggio Emilia; Italia
Fil: Guaitoli, Giorgia. Università di Modena e Reggio Emilia; Italia
Fil: Cerri, Stefania. Università di Modena e Reggio Emilia; Italia
Fil: Dominici, Massimo. Università di Modena e Reggio Emilia; Italia
Fil: Clini, Enrico. Università di Modena e Reggio Emilia; Italia
Materia
CANCER ASSOCIATED FIBROBLASTS (CAFS)
IDIOPATHIC PULMONARY FIBROSIS
LUNG CANCER
MECHANOTRASDUCTION
MYOFIBROBLAST
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/159319
Acceder
id CONICETDig_d7bd541834ed2476b19d8d7819fd7e5a
oai_identifier_str oai:ri.conicet.gov.ar:11336/159319
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Molecular mechanisms and cellular contribution from lung fibrosis to lung cancer developmentSamarelli, Anna ValeriaMasciale, ValentinaAramini, BeatriceColo, Georgina PamelaTonelli, RobertoMarchioni, AlessandroBruzzi, GiuliaGozzi, FilippoAndrisani, DarioCastaniere, IvanaManicardi, LindaMoretti, AntonioTabbì, LucaGuaitoli, GiorgiaCerri, StefaniaDominici, MassimoClini, EnricoCANCER ASSOCIATED FIBROBLASTS (CAFS)IDIOPATHIC PULMONARY FIBROSISLUNG CANCERMECHANOTRASDUCTIONMYOFIBROBLASThttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Idiopathic 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.Fil: Samarelli, Anna Valeria. Università di Modena e Reggio Emilia; ItaliaFil: Masciale, Valentina. Università di Modena e Reggio Emilia; ItaliaFil: Aramini, Beatrice. Università di Modena e Reggio Emilia; Italia. Universidad de Bologna; ItaliaFil: Colo, Georgina Pamela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; ArgentinaFil: Tonelli, Roberto. Università di Modena e Reggio Emilia; ItaliaFil: Marchioni, Alessandro. Università di Modena e Reggio Emilia; ItaliaFil: Bruzzi, Giulia. Università di Modena e Reggio Emilia; ItaliaFil: Gozzi, Filippo. Università di Modena e Reggio Emilia; ItaliaFil: Andrisani, Dario. Università di Modena e Reggio Emilia; ItaliaFil: Castaniere, Ivana. Università di Modena e Reggio Emilia; ItaliaFil: Manicardi, Linda. Università di Modena e Reggio Emilia; ItaliaFil: Moretti, Antonio. Università di Modena e Reggio Emilia; ItaliaFil: Tabbì, Luca. Università di Modena e Reggio Emilia; ItaliaFil: Guaitoli, Giorgia. Università di Modena e Reggio Emilia; ItaliaFil: Cerri, Stefania. Università di Modena e Reggio Emilia; ItaliaFil: Dominici, Massimo. Università di Modena e Reggio Emilia; ItaliaFil: Clini, Enrico. Università di Modena e Reggio Emilia; ItaliaMDPI2021-11-10info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/159319Samarelli, Anna Valeria; Masciale, Valentina; Aramini, Beatrice; Colo, Georgina Pamela; Tonelli, Roberto; et al.; Molecular mechanisms and cellular contribution from lung fibrosis to lung cancer development; MDPI; International Journal of Molecular Sciences; 22; 22; 10-11-2021; 12179-122071661-65961422-0067CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.mdpi.com/1422-0067/22/22/12179info:eu-repo/semantics/altIdentifier/doi/10.3390/ijms222212179info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-15T15:03:27Zoai:ri.conicet.gov.ar:11336/159319instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-10-15 15:03:27.903CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Molecular mechanisms and cellular contribution from lung fibrosis to lung cancer development
title Molecular mechanisms and cellular contribution from lung fibrosis to lung cancer development
spellingShingle Molecular mechanisms and cellular contribution from lung fibrosis to lung cancer development
Samarelli, Anna Valeria
CANCER ASSOCIATED FIBROBLASTS (CAFS)
IDIOPATHIC PULMONARY FIBROSIS
LUNG CANCER
MECHANOTRASDUCTION
MYOFIBROBLAST
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
dc.creator.none.fl_str_mv Samarelli, Anna Valeria
Masciale, Valentina
Aramini, Beatrice
Colo, Georgina Pamela
Tonelli, Roberto
Marchioni, Alessandro
Bruzzi, Giulia
Gozzi, Filippo
Andrisani, Dario
Castaniere, Ivana
Manicardi, Linda
Moretti, Antonio
Tabbì, Luca
Guaitoli, Giorgia
Cerri, Stefania
Dominici, Massimo
Clini, Enrico
author Samarelli, Anna Valeria
author_facet Samarelli, Anna Valeria
Masciale, Valentina
Aramini, Beatrice
Colo, Georgina Pamela
Tonelli, Roberto
Marchioni, Alessandro
Bruzzi, Giulia
Gozzi, Filippo
Andrisani, Dario
Castaniere, Ivana
Manicardi, Linda
Moretti, Antonio
Tabbì, Luca
Guaitoli, Giorgia
Cerri, Stefania
Dominici, Massimo
Clini, Enrico
author_role author
author2 Masciale, Valentina
Aramini, Beatrice
Colo, Georgina Pamela
Tonelli, Roberto
Marchioni, Alessandro
Bruzzi, Giulia
Gozzi, Filippo
Andrisani, Dario
Castaniere, Ivana
Manicardi, Linda
Moretti, Antonio
Tabbì, Luca
Guaitoli, Giorgia
Cerri, Stefania
Dominici, Massimo
Clini, Enrico
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv CANCER ASSOCIATED FIBROBLASTS (CAFS)
IDIOPATHIC PULMONARY FIBROSIS
LUNG CANCER
MECHANOTRASDUCTION
MYOFIBROBLAST
topic CANCER ASSOCIATED FIBROBLASTS (CAFS)
IDIOPATHIC PULMONARY FIBROSIS
LUNG CANCER
MECHANOTRASDUCTION
MYOFIBROBLAST
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv 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.
Fil: Samarelli, Anna Valeria. Università di Modena e Reggio Emilia; Italia
Fil: Masciale, Valentina. Università di Modena e Reggio Emilia; Italia
Fil: Aramini, Beatrice. Università di Modena e Reggio Emilia; Italia. Universidad de Bologna; Italia
Fil: Colo, Georgina Pamela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina
Fil: Tonelli, Roberto. Università di Modena e Reggio Emilia; Italia
Fil: Marchioni, Alessandro. Università di Modena e Reggio Emilia; Italia
Fil: Bruzzi, Giulia. Università di Modena e Reggio Emilia; Italia
Fil: Gozzi, Filippo. Università di Modena e Reggio Emilia; Italia
Fil: Andrisani, Dario. Università di Modena e Reggio Emilia; Italia
Fil: Castaniere, Ivana. Università di Modena e Reggio Emilia; Italia
Fil: Manicardi, Linda. Università di Modena e Reggio Emilia; Italia
Fil: Moretti, Antonio. Università di Modena e Reggio Emilia; Italia
Fil: Tabbì, Luca. Università di Modena e Reggio Emilia; Italia
Fil: Guaitoli, Giorgia. Università di Modena e Reggio Emilia; Italia
Fil: Cerri, Stefania. Università di Modena e Reggio Emilia; Italia
Fil: Dominici, Massimo. Università di Modena e Reggio Emilia; Italia
Fil: Clini, Enrico. Università di Modena e Reggio Emilia; Italia
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.
publishDate 2021
dc.date.none.fl_str_mv 2021-11-10
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/159319
Samarelli, Anna Valeria; Masciale, Valentina; Aramini, Beatrice; Colo, Georgina Pamela; Tonelli, Roberto; et al.; Molecular mechanisms and cellular contribution from lung fibrosis to lung cancer development; MDPI; International Journal of Molecular Sciences; 22; 22; 10-11-2021; 12179-12207
1661-6596
1422-0067
CONICET Digital
CONICET
url http://hdl.handle.net/11336/159319
identifier_str_mv Samarelli, Anna Valeria; Masciale, Valentina; Aramini, Beatrice; Colo, Georgina Pamela; Tonelli, Roberto; et al.; Molecular mechanisms and cellular contribution from lung fibrosis to lung cancer development; MDPI; International Journal of Molecular Sciences; 22; 22; 10-11-2021; 12179-12207
1661-6596
1422-0067
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.mdpi.com/1422-0067/22/22/12179
info:eu-repo/semantics/altIdentifier/doi/10.3390/ijms222212179
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv MDPI
publisher.none.fl_str_mv MDPI
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
_version_ 1846083177248980992
score 13.22299

Publicaciones similares