Related Experiment Video
Updated: Feb 20, 2026

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
Published on: June 6, 2025
Unveiling the epigenetic landscape of AMPK regulation in cancer metabolism
Shweta Dongre1, Arunima Jaiswal1, Megha Chaudhary1
1Department of Biochemistry, Central University of Rajasthan, India.
Abstract:
Cancer cells reprogram their metabolism not only through genetic mutations but also via reversible epigenetic modifications that alter gene expression without changing the DNA sequence. AMP-activated protein kinase (AMPK) is a master regulator of cellular energy homeostasis. It plays a crucial role in cancer by modulating key metabolic pathways, including autophagy, lipid biosynthesis, and glucose utilization. Emerging evidence suggests that AMPK is tightly regulated by epigenetic mechanisms, including DNA methylation, histone remodeling, and non-coding RNAs, which influence AMPK gene expression, activation, and post-translational stability. Non-coding RNAs, including long non-coding RNAs, microRNAs, and circular RNAs, often engage in dynamic feedback loops with AMPK, coupling metabolic stress to transcriptional and epigenetic remodeling. In parallel, DNA methylation and histone modifications influence AMPK signaling indirectly through modulation of upstream regulators and directly via chromatin-associated functions of AMPK. Despite extensive characterization of AMPK function in cancer metabolism, the epigenetic mechanism governing its regulation remain comparatively underexplored. Distinct epigenetic signatures associated with AMPK regulation are being explored as a potential therapeutic target. This review provides a comprehensive overview of epigenetic regulation of AMPK in cancer and highlights its potential in the context of metabolic reprogramming and precision oncology.
Insights
Cancer cells reprogram metabolism via epigenetic changes affecting AMP-activated protein kinase (AMPK). Understanding AMPK
Area of Science:
- Oncology and Molecular Biology
- Cancer Metabolism Research
- Epigenetics and Gene Regulation
Background:
- Cancer cells exhibit metabolic reprogramming through genetic mutations and epigenetic modifications.
- AMP-activated protein kinase (AMPK) is a critical regulator of cellular energy homeostasis and plays a significant role in cancer metabolism.
- Epigenetic mechanisms, including DNA methylation, histone remodeling, and non-coding RNAs, are increasingly recognized as regulators of AMPK.
Purpose of the Study:
- To provide a comprehensive overview of the epigenetic regulation of AMPK in cancer.
- To highlight the role of epigenetic modifications in AMPK-mediated metabolic reprogramming.
- To explore the potential of targeting AMPK epigenetic regulation in precision oncology.
Main Methods:
- Review of existing literature on AMPK function and epigenetic regulation in cancer.
- Analysis of the interplay between non-coding RNAs, DNA methylation, histone modifications, and AMPK signaling.
- Discussion of the implications of AMPK epigenetic regulation in cancer metabolism.
Main Results:
- Emerging evidence indicates that AMPK is tightly controlled by epigenetic mechanisms affecting its gene expression, activation, and stability.
- Non-coding RNAs, DNA methylation, and histone modifications dynamically regulate AMPK signaling pathways.
- Epigenetic signatures governing AMPK regulation are being investigated as potential therapeutic targets.
Conclusions:
- Epigenetic regulation of AMPK is a crucial, yet underexplored, aspect of cancer metabolic reprogramming.
- Targeting the epigenetic control of AMPK offers promising avenues for precision oncology strategies.
- Further research into AMPK epigenetic mechanisms is essential for developing novel cancer therapies.
Related Concept Videos
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
PI3K/mTOR/AKT Signaling Pathway
Epigenetic Regulation
X-chromosome...
Epigenetic Regulation
cAMP-dependent Protein Kinase Pathways
Interactions Between Signaling Pathways
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...

