Epithelial to Mesenchymal Transition: Key Regulator of Pancreatic Ductal Adenocarcinoma Progression and Chemoresistance

Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest malignancies, characterized by aggressive biological behavior and a lack of response to currently available chemotherapy. Emerging evidence has identified epithelial to mesenchymal transition (EMT) as a key driver of PDAC progression an...

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Autores principales:	Kostas Palamaris, Evangelos Felekouras, Stratigoula Sakellariou
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	pancreatic ductal adenocarcinoma epithelial to mesenchymal transition cancer stem cells intratumor heterogeneity tumor microenvironment chemoresistance Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282
Acceso en línea:	https://doaj.org/article/7e5ad0ffe3884d85ae1ff2f7a8f1c09d
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spelling	oai:doaj.org-article:7e5ad0ffe3884d85ae1ff2f7a8f1c09d2021-11-11T15:34:00ZEpithelial to Mesenchymal Transition: Key Regulator of Pancreatic Ductal Adenocarcinoma Progression and Chemoresistance10.3390/cancers132155322072-6694https://doaj.org/article/7e5ad0ffe3884d85ae1ff2f7a8f1c09d2021-11-01T00:00:00Zhttps://www.mdpi.com/2072-6694/13/21/5532https://doaj.org/toc/2072-6694Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest malignancies, characterized by aggressive biological behavior and a lack of response to currently available chemotherapy. Emerging evidence has identified epithelial to mesenchymal transition (EMT) as a key driver of PDAC progression and a central regulator in the development of drug resistance. EMT is a reversible transdifferentiation process controlled by complex interactions between multiple signaling pathways such as TGFb, Wnt, and Notch, which converge to a network of specific transcription factors. Activation of EMT transcriptional reprogramming converts cancer cells of epithelial differentiation into a more mesenchymal phenotypic state. EMT occurrence in pre-invasive pancreatic lesions has been implicated in early PDAC dissemination. Moreover, cancer cell phenotypic plasticity driven by EMT contributes to intratumoral heterogeneity and drug tolerance and is mechanistically associated with the emergence of cells exhibiting cancer stem cells (CSCs) phenotype. In this review we summarize the available data on the signaling cascades regulating EMT and the molecular isnteractions between pancreatic cancer and stromal cells that activate them. In addition, we provide a link between EMT, tumor progression, and chemoresistance in PDAC.Kostas PalamarisEvangelos FelekourasStratigoula SakellariouMDPI AGarticlepancreatic ductal adenocarcinomaepithelial to mesenchymal transitioncancer stem cellsintratumor heterogeneitytumor microenvironmentchemoresistanceNeoplasms. Tumors. Oncology. Including cancer and carcinogensRC254-282ENCancers, Vol 13, Iss 5532, p 5532 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	pancreatic ductal adenocarcinoma epithelial to mesenchymal transition cancer stem cells intratumor heterogeneity tumor microenvironment chemoresistance Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282
spellingShingle	pancreatic ductal adenocarcinoma epithelial to mesenchymal transition cancer stem cells intratumor heterogeneity tumor microenvironment chemoresistance Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282 Kostas Palamaris Evangelos Felekouras Stratigoula Sakellariou Epithelial to Mesenchymal Transition: Key Regulator of Pancreatic Ductal Adenocarcinoma Progression and Chemoresistance
description	Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest malignancies, characterized by aggressive biological behavior and a lack of response to currently available chemotherapy. Emerging evidence has identified epithelial to mesenchymal transition (EMT) as a key driver of PDAC progression and a central regulator in the development of drug resistance. EMT is a reversible transdifferentiation process controlled by complex interactions between multiple signaling pathways such as TGFb, Wnt, and Notch, which converge to a network of specific transcription factors. Activation of EMT transcriptional reprogramming converts cancer cells of epithelial differentiation into a more mesenchymal phenotypic state. EMT occurrence in pre-invasive pancreatic lesions has been implicated in early PDAC dissemination. Moreover, cancer cell phenotypic plasticity driven by EMT contributes to intratumoral heterogeneity and drug tolerance and is mechanistically associated with the emergence of cells exhibiting cancer stem cells (CSCs) phenotype. In this review we summarize the available data on the signaling cascades regulating EMT and the molecular isnteractions between pancreatic cancer and stromal cells that activate them. In addition, we provide a link between EMT, tumor progression, and chemoresistance in PDAC.
format	article
author	Kostas Palamaris Evangelos Felekouras Stratigoula Sakellariou
author_facet	Kostas Palamaris Evangelos Felekouras Stratigoula Sakellariou
author_sort	Kostas Palamaris
title	Epithelial to Mesenchymal Transition: Key Regulator of Pancreatic Ductal Adenocarcinoma Progression and Chemoresistance
title_short	Epithelial to Mesenchymal Transition: Key Regulator of Pancreatic Ductal Adenocarcinoma Progression and Chemoresistance
title_full	Epithelial to Mesenchymal Transition: Key Regulator of Pancreatic Ductal Adenocarcinoma Progression and Chemoresistance
title_fullStr	Epithelial to Mesenchymal Transition: Key Regulator of Pancreatic Ductal Adenocarcinoma Progression and Chemoresistance
title_full_unstemmed	Epithelial to Mesenchymal Transition: Key Regulator of Pancreatic Ductal Adenocarcinoma Progression and Chemoresistance
title_sort	epithelial to mesenchymal transition: key regulator of pancreatic ductal adenocarcinoma progression and chemoresistance
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/7e5ad0ffe3884d85ae1ff2f7a8f1c09d
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Epithelial to Mesenchymal Transition: Key Regulator of Pancreatic Ductal Adenocarcinoma Progression and Chemoresistance

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