Dynamics of epithelial–mesenchymal plasticity driving cancer drug resistance

Epithelial–mesenchymal transition (EMT) promotes several cancers by increasing tumor cell motility, disrupting epithelial cell phenotypes, apical–basal polarity, and intracellular connections, and enhancing tumor resistance to immunotherapy and chemotherapy. Mesenchymal–epithelial transition (MET),...

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Main Authors: Rashmi Bangarh, Reena V. Saini, Adesh K. Saini, Tejveer Singh, Hemant Joshi, Seema Ramniwas, Moyad Shahwan, Hardeep Singh Tuli
Format: Article
Language:English
Published: Elsevier 2025-03-01
Series:Cancer Pathogenesis and Therapy
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Online Access:http://www.sciencedirect.com/science/article/pii/S2949713224000533
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author Rashmi Bangarh
Reena V. Saini
Adesh K. Saini
Tejveer Singh
Hemant Joshi
Seema Ramniwas
Moyad Shahwan
Hardeep Singh Tuli
author_facet Rashmi Bangarh
Reena V. Saini
Adesh K. Saini
Tejveer Singh
Hemant Joshi
Seema Ramniwas
Moyad Shahwan
Hardeep Singh Tuli
author_sort Rashmi Bangarh
collection DOAJ
description Epithelial–mesenchymal transition (EMT) promotes several cancers by increasing tumor cell motility, disrupting epithelial cell phenotypes, apical–basal polarity, and intracellular connections, and enhancing tumor resistance to immunotherapy and chemotherapy. Mesenchymal–epithelial transition (MET), the opposite of EMT, causes tumor metastasis. EMT drives primary tumor cells, whereas MET inhibits them. Importantly, the complex network of EMT includes cell–cell interactions in the tumor microenvironment. Transcription factors, post-translational regulation, cytokine-mediated signaling, and microRNAs control EMT. In this review, we discussed how molecular mechanisms, signaling networks, and epithelial/mesenchymal states affect cancer treatment resistance and the tumor microenvironment. Research on immunotherapy and chemotherapy problems associated with EMT suggests that targeting EMT might be a potential cancer treatment resistance strategy.
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spelling doaj-art-6f52aa7ae6e342fea475d6c2ce1e73082025-08-20T02:53:13ZengElsevierCancer Pathogenesis and Therapy2949-71322025-03-013212012810.1016/j.cpt.2024.07.002Dynamics of epithelial–mesenchymal plasticity driving cancer drug resistanceRashmi Bangarh0Reena V. Saini1Adesh K. Saini2Tejveer Singh3Hemant Joshi4Seema Ramniwas5Moyad Shahwan6Hardeep Singh Tuli7Department of Bio-Sciences and Technology, Maharishi Markandeshwar Engineering College, Maharishi Markandeshwar (Deemed to Be University), Mullana, Ambala 133207, IndiaDepartment of Bio-Sciences and Technology, Maharishi Markandeshwar Engineering College, Maharishi Markandeshwar (Deemed to Be University), Mullana, Ambala 133207, India; Corresponding author: Department of Bio-Sciences and Technology, Maharishi Markandeshwar Engineering College, Maharishi Markandeshwar (Deemed to Be University), Mullana, Ambala 133207, India.Department of Bio-Sciences and Technology, Maharishi Markandeshwar Engineering College, Maharishi Markandeshwar (Deemed to Be University), Mullana, Ambala 133207, IndiaTranslational Oncology Laboratory, Department of Zoology, Hansraj College, Delhi University, New Delhi 110007, IndiaSchool of Biotechnology, Jawaharlal Nehru University, New Delhi 110067, IndiaUniversity Centre for Research and Development, University Institute of Pharmaceutical Sciences, Chandigarh University, Mohali 140413, IndiaDepartment of Clinical Sciences, College of Pharmacy and Health Sciences, Ajman University, Ajman 346, United Arab Emirates; Centre of Medical and Bio-Allied Health Sciences Research, Ajman University, Ajman 346, United Arab EmiratesDepartment of Bio-Sciences and Technology, Maharishi Markandeshwar Engineering College, Maharishi Markandeshwar (Deemed to Be University), Mullana, Ambala 133207, IndiaEpithelial–mesenchymal transition (EMT) promotes several cancers by increasing tumor cell motility, disrupting epithelial cell phenotypes, apical–basal polarity, and intracellular connections, and enhancing tumor resistance to immunotherapy and chemotherapy. Mesenchymal–epithelial transition (MET), the opposite of EMT, causes tumor metastasis. EMT drives primary tumor cells, whereas MET inhibits them. Importantly, the complex network of EMT includes cell–cell interactions in the tumor microenvironment. Transcription factors, post-translational regulation, cytokine-mediated signaling, and microRNAs control EMT. In this review, we discussed how molecular mechanisms, signaling networks, and epithelial/mesenchymal states affect cancer treatment resistance and the tumor microenvironment. Research on immunotherapy and chemotherapy problems associated with EMT suggests that targeting EMT might be a potential cancer treatment resistance strategy.http://www.sciencedirect.com/science/article/pii/S2949713224000533Epithelial–mesenchymal transitionTumor microenvironmentMetastasisCancer drug resistance
spellingShingle Rashmi Bangarh
Reena V. Saini
Adesh K. Saini
Tejveer Singh
Hemant Joshi
Seema Ramniwas
Moyad Shahwan
Hardeep Singh Tuli
Dynamics of epithelial–mesenchymal plasticity driving cancer drug resistance
Cancer Pathogenesis and Therapy
Epithelial–mesenchymal transition
Tumor microenvironment
Metastasis
Cancer drug resistance
title Dynamics of epithelial–mesenchymal plasticity driving cancer drug resistance
title_full Dynamics of epithelial–mesenchymal plasticity driving cancer drug resistance
title_fullStr Dynamics of epithelial–mesenchymal plasticity driving cancer drug resistance
title_full_unstemmed Dynamics of epithelial–mesenchymal plasticity driving cancer drug resistance
title_short Dynamics of epithelial–mesenchymal plasticity driving cancer drug resistance
title_sort dynamics of epithelial mesenchymal plasticity driving cancer drug resistance
topic Epithelial–mesenchymal transition
Tumor microenvironment
Metastasis
Cancer drug resistance
url http://www.sciencedirect.com/science/article/pii/S2949713224000533
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