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Association of the Epithelial–Mesenchymal Transition (EMT) with Cisplatin Resistance
Therapy resistance is a characteristic of cancer cells that significantly reduces the effectiveness of drugs. Despite the popularity of cisplatin (CP) as a chemotherapeutic agent, which is widely used in the treatment of various types of cancer, resistance of cancer cells to CP chemotherapy has been...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7312011/ https://www.ncbi.nlm.nih.gov/pubmed/32503307 http://dx.doi.org/10.3390/ijms21114002 |
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author | Ashrafizadeh, Milad Zarrabi, Ali Hushmandi, Kiavash Kalantari, Mahshad Mohammadinejad, Reza Javaheri, Tahereh Sethi, Gautam |
author_facet | Ashrafizadeh, Milad Zarrabi, Ali Hushmandi, Kiavash Kalantari, Mahshad Mohammadinejad, Reza Javaheri, Tahereh Sethi, Gautam |
author_sort | Ashrafizadeh, Milad |
collection | PubMed |
description | Therapy resistance is a characteristic of cancer cells that significantly reduces the effectiveness of drugs. Despite the popularity of cisplatin (CP) as a chemotherapeutic agent, which is widely used in the treatment of various types of cancer, resistance of cancer cells to CP chemotherapy has been extensively observed. Among various reported mechanism(s), the epithelial–mesenchymal transition (EMT) process can significantly contribute to chemoresistance by converting the motionless epithelial cells into mobile mesenchymal cells and altering cell–cell adhesion as well as the cellular extracellular matrix, leading to invasion of tumor cells. By analyzing the impact of the different molecular pathways such as microRNAs, long non-coding RNAs, nuclear factor-κB (NF-ĸB), phosphoinositide 3-kinase-related protein kinase (PI3K)/Akt, mammalian target rapamycin (mTOR), and Wnt, which play an important role in resistance exhibited to CP therapy, we first give an introduction about the EMT mechanism and its role in drug resistance. We then focus specifically on the molecular pathways involved in drug resistance and the pharmacological strategies that can be used to mitigate this resistance. Overall, we highlight the various targeted signaling pathways that could be considered in future studies to pave the way for the inhibition of EMT-mediated resistance displayed by tumor cells in response to CP exposure. |
format | Online Article Text |
id | pubmed-7312011 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-73120112020-06-25 Association of the Epithelial–Mesenchymal Transition (EMT) with Cisplatin Resistance Ashrafizadeh, Milad Zarrabi, Ali Hushmandi, Kiavash Kalantari, Mahshad Mohammadinejad, Reza Javaheri, Tahereh Sethi, Gautam Int J Mol Sci Review Therapy resistance is a characteristic of cancer cells that significantly reduces the effectiveness of drugs. Despite the popularity of cisplatin (CP) as a chemotherapeutic agent, which is widely used in the treatment of various types of cancer, resistance of cancer cells to CP chemotherapy has been extensively observed. Among various reported mechanism(s), the epithelial–mesenchymal transition (EMT) process can significantly contribute to chemoresistance by converting the motionless epithelial cells into mobile mesenchymal cells and altering cell–cell adhesion as well as the cellular extracellular matrix, leading to invasion of tumor cells. By analyzing the impact of the different molecular pathways such as microRNAs, long non-coding RNAs, nuclear factor-κB (NF-ĸB), phosphoinositide 3-kinase-related protein kinase (PI3K)/Akt, mammalian target rapamycin (mTOR), and Wnt, which play an important role in resistance exhibited to CP therapy, we first give an introduction about the EMT mechanism and its role in drug resistance. We then focus specifically on the molecular pathways involved in drug resistance and the pharmacological strategies that can be used to mitigate this resistance. Overall, we highlight the various targeted signaling pathways that could be considered in future studies to pave the way for the inhibition of EMT-mediated resistance displayed by tumor cells in response to CP exposure. MDPI 2020-06-03 /pmc/articles/PMC7312011/ /pubmed/32503307 http://dx.doi.org/10.3390/ijms21114002 Text en © 2020 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 Ashrafizadeh, Milad Zarrabi, Ali Hushmandi, Kiavash Kalantari, Mahshad Mohammadinejad, Reza Javaheri, Tahereh Sethi, Gautam Association of the Epithelial–Mesenchymal Transition (EMT) with Cisplatin Resistance |
title | Association of the Epithelial–Mesenchymal Transition (EMT) with Cisplatin Resistance |
title_full | Association of the Epithelial–Mesenchymal Transition (EMT) with Cisplatin Resistance |
title_fullStr | Association of the Epithelial–Mesenchymal Transition (EMT) with Cisplatin Resistance |
title_full_unstemmed | Association of the Epithelial–Mesenchymal Transition (EMT) with Cisplatin Resistance |
title_short | Association of the Epithelial–Mesenchymal Transition (EMT) with Cisplatin Resistance |
title_sort | association of the epithelial–mesenchymal transition (emt) with cisplatin resistance |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7312011/ https://www.ncbi.nlm.nih.gov/pubmed/32503307 http://dx.doi.org/10.3390/ijms21114002 |
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