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

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

更新时间：2022-06-24

- Metabolic reprogram associated with epithelial-mesenchymal transition in tumor progression and metastasis
- Genes & Diseases Vol. 7, Issue 2, (2020)
- 作者机构：
  
  1. Cancer Institute of Integrative Medicine, Zhejiang Academy of Traditional Chinese Medicine,Zhejiang,Hangzhou,China,310012
  2. Department of Pathology and Pathophysiology, Department of Surgical Oncology (Breast Center) of the Second Affiliated Hospital, Zhejiang University School of Medicine,Hangzhou,China,310058
  3. Departments of Molecular and Cellular Biochemistry, Markey Cancer Center, University of Kentucky School of Medicine,KY,Lexington,USA,40506
- 作者简介：
- 基金信息：
- DOI：10.1016/j.gendis.2019.09.012
  CLC：
- Published：2020，
  
  Published Online：1 June 2020，
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Yifan Wang, Chenfang Dong, Binhua P. Zhou. Metabolic reprogram associated with epithelial-mesenchymal transition in tumor progression and metastasis. [J]. Genes & Diseases 7(2).(2020)
DOI：

Yifan Wang, Chenfang Dong, Binhua P. Zhou. Metabolic reprogram associated with epithelial-mesenchymal transition in tumor progression and metastasis. [J]. Genes & Diseases 7(2).(2020) DOI： 10.1016/j.gendis.2019.09.012.

摘要

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.

关键词

Keywords

EpigeneticsEpithelial-mesenchymal transitionHeterogeneityMetabolismPlasticity

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