ArticleJournal of cell science2018
AMP-activated protein kinase promotes epithelial-mesenchymal transition in cancer cells through Twist1 upregulation.
Article in Journal of cell science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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.
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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.
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Who cites it
33 citing papers in PubMed, 59 citations in OpenAlex.
- EDIL3/Del-1-Dependent Induction of AMPKβ Phosphorylation Regulates the Progression of Mesenchymal Stem-like Triple-Negative Breast Cancer.International journal of molecular sciences · 2026Article
- Dynamic feedback between IL-6 and TWIST1 drives pancreatic cancer progression.Translational gastroenterology and hepatology · 2026Article
- NARI-29: A Novel Epalrestat Derivative Attenuates Pulmonary Fibrosis by Modulating the TGF-β/Smad Signaling.ACS pharmacology & translational science · 2025Article
- Rethinking AMPK: A Reversible Switch Fortifying Cancer Cell Stress-Resilience.The Yale journal of biology and medicine · 2025Review
- Orchestrated desaturation reprogramming from stearoyl-CoA desaturase to fatty acid desaturase 2 in cancer epithelial-mesenchymal transition and metastasis.Cancer communications (London, England) · 2025Article
- Epicardial EMT and cardiac repair: an update.Stem cell research & therapy · 2024Review
- Contribution of Autophagy to Epithelial Mesenchymal Transition Induction during Cancer Progression.Cancers · 2024Review
- Inhibition of protein translation under matrix-deprivation stress in breast cancer cells.Frontiers in medicine · 2023Article
- Markers of Bronchiolitis Obliterans Syndrome after Lung Transplant: Between Old Knowledge and Future Perspective.Biomedicines · 2022Review
- AMPK promotes Arf6 activation in a kinase-independent manner upon glucose starvation.Journal of cell science · 2022Article
- Sirtuins and Hypoxia in EMT Control.Pharmaceuticals (Basel, Switzerland) · 2022Review
- AMP-activated protein kinase promotes breast cancer stemness and drug resistance.Disease models & mechanisms · 2022Article
- Tumor Cell Glycolysis-At the Crossroad of Epithelial-Mesenchymal Transition and Autophagy.Cells · 2022Review
- Epithelial-to-Mesenchymal Transition Signaling Pathways Responsible for Breast Cancer Metastasis.Cellular and molecular bioengineering · 2022Review
- The impact of serum-free culture on HEK293 cells: From the establishment of suspension and adherent serum-free adaptation cultures to the investigation of growth and metabolic profiles.Frontiers in bioengineering and biotechnology · 2022Article
- Extracellular Vesicles Mediate Immune Responses to Tissue-Associated Self-Antigens: Role in Solid Organ Transplantations.Frontiers in immunology · 2022Review
- Inflammatory Breast Cancer: The Secretome of HCMVFrontiers in oncology · 2022Article
- The crosstalk within the breast tumor microenvironment in type II diabetes: Implications for cancer disparities.Frontiers in endocrinology · 2022Review
- Copper depletion modulates mitochondrial oxidative phosphorylation to impair triple negative breast cancer metastasis.Nature communications · 2021Article
- The mitochondrially-localized nucleoside diphosphate kinase D (NME4) is a novel metastasis suppressor.BMC biology · 2021Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The developmental programme of epithelial-mesenchymal transition (EMT), involving loss of epithelial and acquisition of mesenchymal properties, plays an important role in the invasion-metastasis cascade of cancer cells. In the present study, we show that activation of AMP-activated protein kinase (AMPK) using A769662 led to a concomitant induction of EMT in multiple cancer cell types, as observed by enhanced expression of mesenchymal markers, decrease in epithelial markers, and increase in migration and invasion. In contrast, inhibition or depletion of AMPK led to a reversal of EMT. Importantly, AMPK activity was found to be necessary for the induction of EMT by physiological cues such as hypoxia and TGFβ treatment. Furthermore, AMPK activation increased the expression and nuclear localization of Twist1, an EMT transcription factor. Depletion of Twist1 impaired AMPK-induced EMT phenotypes, suggesting that AMPK might mediate its effects on EMT, at least in part, through Twist1 upregulation. Inhibition or depletion of AMPK also attenuated metastasis. Thus, our data underscore a central role for AMPK in the induction of EMT and in metastasis, suggesting that strategies targeting AMPK might provide novel approaches to curb cancer spread.
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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.