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 | |
| State | Published - Jun 2020 |
Bibliographical note
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