ArticleJournal of cellular and molecular medicine2020
Low levels of AMPK promote epithelial-mesenchymal transition in lung cancer primarily through HDAC4- and HDAC5-mediated metabolic reprogramming.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- HDAC4 Promotes Cancer Stemness in Nonsmall Cell Lung Cancer by Upregulating SLC38A2 Expression via HIF-1α to Enhance Glutamine Metabolism.Analytical cellular pathology (Amsterdam) · 2026Article
- Thermal shift engagement assay for Class IIA histone deacetylase inhibitor screening.Results in chemistry · 2025Article
- Elevated meteorin-like protein from high-intensity interval training improves heart function via AMPK/HDAC4 pathway.Genes & diseases · 2024Article
- Temporal regulation of acetylation status determines PARP1 role in DNA damage response and metabolic homeostasis.Science advances · 2024Article
- Sex-related DNA methylation is associated with inflammation and gene expression in the lungs of healthy individuals.Scientific reports · 2024Article
- Decoding the coupled decision-making of the epithelial-mesenchymal transition and metabolic reprogramming in cancer.iScience · 2023Article
- RBMS3, a downstream target of AMPK, Exerts Inhibitory Effects on Invasion and Metastasis of Lung Cancer.Journal of Cancer · 2023Article
- HDAC4 in cancer: A multitasking platform to drive not only epigenetic modifications.Frontiers in molecular biosciences · 2023Review
- Inspiratory hyperoxia suppresses lung cancer metastasis through a MYC/SLC1A5-dependent metabolic pathway.The European respiratory journal · 2022Article
- Article
- Novel long non-coding RNA CYB561-5 promotes aerobic glycolysis and tumorigenesis by interacting with basigin in non-small cell lung cancer.Journal of cellular and molecular medicine · 2022Article
- Free Fatty Acid Impairs Myogenic Differentiation through the AMPKα-MicroRNA 206 Pathway.Molecular and cellular biology · 2022Article
- The Epithelial-Mesenchymal Transition at the Crossroads between Metabolism and Tumor Progression.International journal of molecular sciences · 2022Review
- Senescence marker protein 30 inhibits tumor growth by reducing HDAC4 expression in non-small cell lung cancer.Translational lung cancer research · 2021Article
- A Prognostic Model for Brain Glioma Patients Based on 9 Signature Glycolytic Genes.BioMed research international · 2021Article
- Insights Into the Function and Clinical Application of HDAC5 in Cancer Management.Frontiers in oncology · 2021Review
- Low levels of AMPK promote epithelial-mesenchymal transition in lung cancer primarily through HDAC4- and HDAC5-mediated metabolic reprogramming.Journal of cellular and molecular medicine · 2020Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AMP-activated protein kinase (AMPK) serves as a "supermetabolic regulator" that helps maintain cellular energy homeostasis. However, the role of AMPK in glucose metabolism reprogramming in lung cancer remains unclear. Here, our study shows that low AMPK expression correlates with metastasis and clinicopathologic parameters of non-small-cell lung cancer. Low AMPK significantly enhances the Warburg effect in HBE and A549 cells, which in turn induces the expression of mesenchymal markers and enhances their invasion and migration. At the mechanistic level, low AMPK up-regulates HK2 expression and glycolysis levels through HDAC4 and HDAC5. Collectively, our findings demonstrate that low AMPK-induced metabolism can promote epithelial-mesenchymal transition progression in normal bronchial epithelial cells and lung cancer cells, and increase the risk for tumour metastasis.
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