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Updated: Jun 27, 2026
11:42
Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
Published on: April 7, 2017
Bidirectional Feedback Between Metabolic Reprogramming and Epithelial-Mesenchymal Transition: From Mechanisms to
Yuxin Liu1, Mengke Wang1, Dan Liu1
1College of Basic Medicine, Heilongjiang University of Chinese Medicine, Harbin 150040, China.
Molecules (Basel, Switzerland)
|June 26, 2026
Summary
Tumor metastasis involves epithelial-mesenchymal transition (EMT) and metabolic reprogramming. This review explores how cancer cells alter metabolism to support EMT, driving disease progression and offering therapeutic targets.
Area of Science:
- Oncology
- Cancer Metabolism
- Cellular Biology
Background:
- Tumor metastasis is a major cause of cancer mortality.
- Epithelial-mesenchymal transition (EMT) is crucial for cancer cell dissemination.
- Cancer cells undergoing EMT exhibit significant metabolic reprogramming.
Purpose of the Study:
- To review the bidirectional relationship between EMT and metabolic reprogramming.
- To examine the implications of this crosstalk in cancer progression.
- To summarize therapeutic strategies targeting this interplay.
Main Methods:
- Systematic literature review.
- Analysis of metabolic pathways involved in EMT.
- Examination of signaling and epigenetic modifications.
Main Results:
- EMT is supported by altered glycolysis, oxidative phosphorylation, lipid, and amino acid metabolism.
- Metabolic intermediates influence EMT progression via signaling and epigenetics.
- This crosstalk is integral to neoplastic disease progression.
Conclusions:
- The interplay between EMT and metabolism is a key driver of cancer metastasis.
- Targeting metabolic reprogramming in EMT offers promising therapeutic avenues.
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