Biological role of metabolic reprogramming of cancer cells during epithelial‑mesenchymal transition (Review)

Abstract

Epithelial-mesenchymal transition (EMT) is required for the distant metastasis of tumors. The degree of tumor malignancy increases as EMT progresses. Notably, the biology of tumor cells differs from that of normal cells, with regards to characteristics and energy metabolism mechanisms; abnormal glucose metabolism, excessive accumulation of fatty acids and other metabolic disorders occur in metastatic tumors. Previous studies have confirmed that the regulation of tumor cell metabolism can affect tumor metastasis and some findings have resulted in novel clinical applications. The present review aimed to provide a basis for treatments targeting the tumor EMT process and metabolic reprogramming. Contents 1. Introduction 2. The EMT process and cancer progression 3. Metabolism and EMT 4. Glucose metabolism during EMT 5. Lipid metabolism during EMT 6. Amino acid metabolism during EMT 7. Nucleic acid metabolism during EMT 8. Enzymes and EMT 9. EMT and CSCs 10. Metabolism-associated oncogenes and tumor-suppressor genes 11. Conclusion and prospects

Glutamine-Fructose-6-Phosphate Transaminase 2 (GFPT2) Is Upregulated in Breast Epithelial–Mesenchymal Transition and Responds to Oxidative Stress

“…Both the LFQ and SILAC data indicated D492HER2 as a "mesenchymal-like/claudin-low" cell type showing the most similarity to the tumorigenic MDA-MB-157 cells originally isolated from metastatic human breast carcinoma (59,61,63). Given the basal origin of D492, the relatively small changes to the coverage of the proteome between these cell lines (5-7 %), and that the claudin-low phenotype has recently been re-defined as a molecular signature found dispersed within the intrinsic breast cancer subtypes Focusing on metabolism, a variety of metabolic enzymes involved in a diversity of metabolic pathways were significantly altered in EMT according to our data, supporting that EMT is entangled with the metabolic network, e.g., central carbon metabolism including glycolysis and oxidative phosphorylation, pentose phosphate pathway (PPP), and mitochondrial metabolism, lipid metabolism, glutamine metabolism, nucleotide metabolism, and glycan metabolism (65). The upregulation of PGM3, UAP1, and OGT, also components of the HBP in the mesenchymal cells supports the increased activities of HBP in EMT.…”

Identification and validation of an immune signature associated with EMT and metabolic reprogramming for predicting prognosis and drug response in bladder cancer

“…Metabolic reprogramming of tumors refers to the construction of a completely new metabolic network under the aberrant expression of oncogenes, which redefines the flow of nutrients and energy in the metabolic network during tumorigenesis (M. 21 ). Metabolic reprogramming is an important pathway that mediates EMT while itself being strictly regulated by EMT-related factors.…”

<p>OGDH promotes the progression of gastric cancer by regulating mitochondrial bioenergetics and Wnt/β-catenin signal pathway</p>

“…The silencing of FBP1 favours EMT in gastric cells in vitro 30. EMT also is a key signature of tumours harbouring mutations in the TCA cycle enzymes FH, SDH and IDH 31. OGDHC inhibitor AA6 inhibits breast cancer-associated metastasis by regulating 2-OG-dependent TET-miR200-Zeb1/CtBP1-MMP3 axis 15.…”