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Metabolic reprogram associated with epithelial-mesenchymal transition in tumor progression and metastasis

Epithelial-mesenchymal Transition (EMT) is a de-differentiation program that imparts tumor cells with the phenotypic and cellular plasticity required for drug resistance, metastasis, and recurrence. This dynamic and reversible events is governed by a network of EMT-transcription factors (EMT-TFs) th...

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Detalles Bibliográficos
Autores principales: Wang, Yifan, Dong, Chenfang, Zhou, Binhua P.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Chongqing Medical University 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7083713/
https://www.ncbi.nlm.nih.gov/pubmed/32215287
http://dx.doi.org/10.1016/j.gendis.2019.09.012
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author Wang, Yifan
Dong, Chenfang
Zhou, Binhua P.
author_facet Wang, Yifan
Dong, Chenfang
Zhou, Binhua P.
author_sort Wang, Yifan
collection PubMed
description Epithelial-mesenchymal Transition (EMT) is a de-differentiation program that imparts tumor cells with the phenotypic and cellular plasticity required for drug resistance, metastasis, and recurrence. This dynamic and reversible events is governed by a network of EMT-transcription factors (EMT-TFs) through epigenetic regulation. Many chromatin modifying-enzymes utilize metabolic intermediates as cofactors or substrates; this suggests that EMT is subjected to the metabolic regulation. Conversely, EMT rewires metabolic program to accommodate cellular changes during EMT. Here we summarize the latest findings regarding the epigenetic regulation of EMT, and discuss the mutual interactions among metabolism, epigenetic regulation, and EMT. Finally, we provide perspectives of how this interplay contributes to cellular plasticity, which may result in the clinical manifestation of tumor heterogeneity.
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spelling pubmed-70837132020-03-25 Metabolic reprogram associated with epithelial-mesenchymal transition in tumor progression and metastasis Wang, Yifan Dong, Chenfang Zhou, Binhua P. Genes Dis Article Epithelial-mesenchymal Transition (EMT) is a de-differentiation program that imparts tumor cells with the phenotypic and cellular plasticity required for drug resistance, metastasis, and recurrence. This dynamic and reversible events is governed by a network of EMT-transcription factors (EMT-TFs) through epigenetic regulation. Many chromatin modifying-enzymes utilize metabolic intermediates as cofactors or substrates; this suggests that EMT is subjected to the metabolic regulation. Conversely, EMT rewires metabolic program to accommodate cellular changes during EMT. Here we summarize the latest findings regarding the epigenetic regulation of EMT, and discuss the mutual interactions among metabolism, epigenetic regulation, and EMT. Finally, we provide perspectives of how this interplay contributes to cellular plasticity, which may result in the clinical manifestation of tumor heterogeneity. Chongqing Medical University 2019-10-03 /pmc/articles/PMC7083713/ /pubmed/32215287 http://dx.doi.org/10.1016/j.gendis.2019.09.012 Text en © 2019 Chongqing Medical University. Production and hosting by Elsevier B.V. http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Article
Wang, Yifan
Dong, Chenfang
Zhou, Binhua P.
Metabolic reprogram associated with epithelial-mesenchymal transition in tumor progression and metastasis
title Metabolic reprogram associated with epithelial-mesenchymal transition in tumor progression and metastasis
title_full Metabolic reprogram associated with epithelial-mesenchymal transition in tumor progression and metastasis
title_fullStr Metabolic reprogram associated with epithelial-mesenchymal transition in tumor progression and metastasis
title_full_unstemmed Metabolic reprogram associated with epithelial-mesenchymal transition in tumor progression and metastasis
title_short Metabolic reprogram associated with epithelial-mesenchymal transition in tumor progression and metastasis
title_sort metabolic reprogram associated with epithelial-mesenchymal transition in tumor progression and metastasis
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7083713/
https://www.ncbi.nlm.nih.gov/pubmed/32215287
http://dx.doi.org/10.1016/j.gendis.2019.09.012
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