ReviewGenes & diseases2020
Metabolic reprogram associated with epithelial-mesenchymal transition in tumor progression and metastasis.
Review in Genes & diseases, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 41 citations in OpenAlex.
- Cancer stem cells and drug resistance in cancer: molecular mechanisms and therapeutic targets.Molecular biomedicine · 2026Review
- Bidirectional Feedback Between Metabolic Reprogramming and Epithelial-Mesenchymal Transition: From Mechanisms to Therapeutic Interventions.Molecules (Basel, Switzerland) · 2026Review
- USP5 in cancer: a therapeutic window into metabolism and drug resistance.Journal of translational medicine · 2026Review
- Loss of protein phosphatase 1 regulator TIMAP protein triggers EMT in A549 cells.Cell communication and signaling : CCS · 2026Article
- An epithelial-mesenchymal transition-related gene signature predicts prognosis, immune infiltration, and drug sensitivity in colorectal cancer.Cancer drug resistance (Alhambra, Calif.) · 2026Article
- Aspirin-Inspired 6-O-Carboxymethyl-N-Acetylglucosamine: A potent antitumor agent with enhanced efficacy.Apoptosis : an international journal on programmed cell death · 2025Article
- Lipid metabolism in cancer stem cells: reprogramming, mechanisms, crosstalk, and therapeutic approaches.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Epithelial-mesenchymal transition in colorectal cancer metastasis and progression: molecular mechanisms and therapeutic strategies.Cell death discovery · 2025Review
- Single-nucleus CUT&RUN elucidates the function of intrinsic and genomics-driven epigenetic heterogeneity in head and neck cancer progression.Genome research · 2025Article
- The impact of epithelial-mesenchymal transition (EMT) induced by metabolic processes and intracellular signaling pathways on chemo-resistance, metastasis, and recurrence in solid tumors.Cell communication and signaling : CCS · 2024Review
- The crosstalk role of CDKN2A between tumor progression and cuproptosis resistance in colorectal cancer.Aging · 2024Article
- Regulation of mitochondrial metabolism by autophagy supports leptin-induced cell migration.Scientific reports · 2024Article
- Histone modifications and their roles in macrophage-mediated inflammation: a new target for diabetic wound healing.Frontiers in immunology · 2024Review
- SSPH I, A Novel Anti-cancer Saponin, Inhibits EMT and Invasion and Migration of NSCLC by Suppressing MAPK/ERK1/2 and PI3K/AKT/ mTOR Signaling Pathways.Recent patents on anti-cancer drug discovery · 2024Article
- Ets1 facilitates EMT/invasion through Drp1-mediated mitochondrial fragmentation in ovarian cancer.iScience · 2023Article
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- Review
- Cytokine signaling converging onFrontiers in immunology · 2023Article
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- Investigating the Function of Human Jumping Translocation Breakpoint Protein (hJTB) and Its Interacting Partners through In-Solution Proteomics of MCF7 Cells.Molecules (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.