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

Yifan Wang; Chenfang Dong; Binhua P. Zhou

doi:10.1016/j.gendis.2019.09.012

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

Yifan Wang, Chenfang Dong, Binhua P. Zhou

Research output: Contribution to journal › Review article › peer-review

17 Scopus citations

Abstract

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.

Original language	English
Pages (from-to)	172-184
Number of pages	13
Journal	Genes and Diseases
Volume	7
Issue number	2
DOIs	https://doi.org/10.1016/j.gendis.2019.09.012
State	Published - Jun 2020

Bibliographical note

Funding Information:
We apologize to the many contributors to this field whose work are important while we were unable to cite due to space limitation. Our study is supported by the grants from National Institutes of Health (NIH) ( RO1s CA125454 and CA188118 ), Department of Defense (DOD) Breakthrough Award ( BC140733P1 ), Mary Kay Ash Foundation (to B.P. Zhou), and the Basic Public Welfare Research Program of Zhejiang Province ( LGF18H290003 to Y. Wang).

Funding Information:
We apologize to the many contributors to this field whose work are important while we were unable to cite due to space limitation. Our study is supported by the grants from National Institutes of Health (NIH) (RO1s CA125454 and CA188118), Department of Defense (DOD) Breakthrough Award (BC140733P1), Mary Kay Ash Foundation (to B.P. Zhou), and the Basic Public Welfare Research Program of Zhejiang Province (LGF18H290003 to Y. Wang).

Publisher Copyright:
© 2019 Chongqing Medical University

Keywords

Epigenetics
Epithelial-mesenchymal transition
Heterogeneity
Metabolism
Plasticity

ASJC Scopus subject areas

Biochemistry
Molecular Biology
Genetics(clinical)
Cell Biology

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10.1016/j.gendis.2019.09.012

Cite this

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title = "Metabolic reprogram associated with epithelial-mesenchymal transition in tumor progression and metastasis",

abstract = "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.",

keywords = "Epigenetics, Epithelial-mesenchymal transition, Heterogeneity, Metabolism, Plasticity",

author = "Yifan Wang and Chenfang Dong and Zhou, {Binhua P.}",

note = "Funding Information: We apologize to the many contributors to this field whose work are important while we were unable to cite due to space limitation. Our study is supported by the grants from National Institutes of Health (NIH) ( RO1s CA125454 and CA188118 ), Department of Defense (DOD) Breakthrough Award ( BC140733P1 ), Mary Kay Ash Foundation (to B.P. Zhou), and the Basic Public Welfare Research Program of Zhejiang Province ( LGF18H290003 to Y. Wang). Funding Information: We apologize to the many contributors to this field whose work are important while we were unable to cite due to space limitation. Our study is supported by the grants from National Institutes of Health (NIH) (RO1s CA125454 and CA188118), Department of Defense (DOD) Breakthrough Award (BC140733P1), Mary Kay Ash Foundation (to B.P. Zhou), and the Basic Public Welfare Research Program of Zhejiang Province (LGF18H290003 to Y. Wang). Publisher Copyright: {\textcopyright} 2019 Chongqing Medical University",

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N1 - Funding Information: We apologize to the many contributors to this field whose work are important while we were unable to cite due to space limitation. Our study is supported by the grants from National Institutes of Health (NIH) ( RO1s CA125454 and CA188118 ), Department of Defense (DOD) Breakthrough Award ( BC140733P1 ), Mary Kay Ash Foundation (to B.P. Zhou), and the Basic Public Welfare Research Program of Zhejiang Province ( LGF18H290003 to Y. Wang). Funding Information: We apologize to the many contributors to this field whose work are important while we were unable to cite due to space limitation. Our study is supported by the grants from National Institutes of Health (NIH) (RO1s CA125454 and CA188118), Department of Defense (DOD) Breakthrough Award (BC140733P1), Mary Kay Ash Foundation (to B.P. Zhou), and the Basic Public Welfare Research Program of Zhejiang Province (LGF18H290003 to Y. Wang). Publisher Copyright: © 2019 Chongqing Medical University

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N2 - 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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Metabolic reprogram associated with epithelial-mesenchymal transition in tumor progression and metastasis

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

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