ReviewFrontiers in cell and developmental biology2017
MYC and AMPK-Save Energy or Die!
Review in Frontiers in cell and developmental biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
25 citing papers in PubMed, 25 citations in OpenAlex.
- PPRC1 is a prognostic biomarker and key regulator of mitochondrial oxidative phosphorylation in multiple myeloma.Annals of medicine · 2026Article
- Transient MYC Mimicking the Exercise Response Orchestrates Multifaceted Skeletal Muscle Adaptations.bioRxiv : the preprint server for biology · 2026Article
- FGF19 in Solid Tumors: Molecular Mechanisms, Metabolic Reprogramming, and Emerging Therapeutic Opportunities.Theranostics · 2026Review
- Metabolic Reprogramming of Anti-cancer T Cells: Targeting AMPK and PPAR to Optimize Cancer Immunotherapy.Indian journal of clinical biochemistry : IJCB · 2025Review
- Article
- Network pharmacology-based study on the mechanism of Tangfukang formula against type 2 diabetes mellitus.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- Association of glutaminase expression with immune-suppressive tumor microenvironment, clinicopathologic features, and clinical outcomes in endometrial cancer.International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · 2024Article
- Plasma Proteomic Kinetics in Response to Acute Exercise.Molecular & cellular proteomics : MCP · 2023Article
- Mitochondrial complex III deficiency drives c-MYC overexpression and illicit cell cycle entry leading to senescence and segmental progeria.Nature communications · 2023Article
- Improved antitumor activity against prostate cancer via synergistic targeting of Myc and GFAT-1.Theranostics · 2023Article
- MYC-an emerging player in mitochondrial diseases.Frontiers in cell and developmental biology · 2023Review
- Reprogramming of glutamine metabolism and its impact on immune response in the tumor microenvironment.Cell communication and signaling : CCS · 2022Review
- Bone morphogenetic protein inhibitors and mitochondria targeting agents synergistically induce apoptosis-inducing factor (AIF) caspase-independent cell death in lung cancer cells.Cell communication and signaling : CCS · 2022Article
- B-cell Receptor Signaling Induced Metabolic Alterations in Chronic Lymphocytic Leukemia Can Be Partially Bypassed byHemaSphere · 2022Article
- Cyclin-Dependent Kinase Synthetic Lethality Partners in DNA Damage Response.International journal of molecular sciences · 2022Review
- Translating MSC Therapy in the Age of Obesity.Frontiers in immunology · 2022Review
- Barriers to Immunotherapy in Ovarian Cancer: Metabolic, Genomic, and Immune Perturbations in the Tumour Microenvironment.Cancers · 2021Review
- The potent AMPK inhibitor BAY-3827 shows strong efficacy in androgen-dependent prostate cancer models.Cellular oncology (Dordrecht, Netherlands) · 2021Article
- Revisiting lactate dynamics in cancer-a metabolic expertise or an alternative attempt to survive?Journal of molecular medicine (Berlin, Germany) · 2020Review
- Defining a metabolic landscape of tumours: genome meets metabolism.British journal of cancer · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MYC sustains non-stop proliferation by altering metabolic machinery to support growth of cell mass. As part of the metabolic transformation MYC promotes lipid, nucleotide and protein synthesis by hijacking citric acid cycle to serve biosynthetic processes, which simultaneously exhausts ATP production. This leads to the activation of cellular energy sensing protein, AMP-activated protein kinase (AMPK). Cells with normal growth control can stop cell proliferation machinery to replenish ATP reservoirs whereas MYC prevents such break by blocking the cell cycle exit. The relentless cell cycle activation, accompanied by sustained metabolic stress and AMPK activity, switches the energy-saving AMPK to pro-apoptotic AMPK. The AMPK-involving metabolic side of MYC apoptosis may provide novel avenues for therapeutic development. Here we first review the role of anabolic MYC and catabolic AMPK pathways in context of cancer and then discuss how the concomitant activity of both pathways in tumor cells may result in targetable synthetic lethal vulnerabilities.
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What OpenQuestion holds
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.