
Several lines of evidence indicate that during transformation epithelial cancer cells can acquire mesenchymal features via a process called epithelial‐to‐mesenchymal transition (EMT). This process endows cancer cells with increased invasive and migratory capacity, enabling tumour dissemination and metastasis. EMT is associated with a complex metabolic reprogramming, orchestrated by EMT transcription factors, which support the energy requirements of increased motility and growth in harsh environmental conditions. The discovery that mutations in metabolic genes such as FH, SDH and IDH activate EMT provided further evidence that EMT and metabolism are intertwined. In this review, we discuss the role of EMT in cancer and the underpinning metabolic reprogramming. We also put forward the hypothesis that, by altering chromatin structure and function, metabolic pathways engaged by EMT are necessary for its full activation.
IDH, Epithelial-Mesenchymal Transition, mitochondrial metabolism, SDH, FH, Fumarate Hydratase, Cell Movement, Neoplasms, Humans, cancer, metastasis, Neoplasm Invasiveness, epigenetics, EMT, Cellular Reprogramming, Chromatin, Isocitrate Dehydrogenase, Gene Expression Regulation, Neoplastic, Succinate Dehydrogenase, Cell Transformation, Neoplastic, Mutation, Neoplastic Stem Cells, metabolism, Metabolic Networks and Pathways, Transcription Factors
IDH, Epithelial-Mesenchymal Transition, mitochondrial metabolism, SDH, FH, Fumarate Hydratase, Cell Movement, Neoplasms, Humans, cancer, metastasis, Neoplasm Invasiveness, epigenetics, EMT, Cellular Reprogramming, Chromatin, Isocitrate Dehydrogenase, Gene Expression Regulation, Neoplastic, Succinate Dehydrogenase, Cell Transformation, Neoplastic, Mutation, Neoplastic Stem Cells, metabolism, Metabolic Networks and Pathways, Transcription Factors
| selected citations These citations are derived from selected sources. This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | 276 | |
| popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network. | Top 1% | |
| influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | Top 10% | |
| impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network. | Top 0.1% |
