ArticleMolecular oncology2017
AMPK β1 reduces tumor progression and improves survival in p53 null mice.
Article in Molecular oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Phytochemicals regulate cancer metabolism through modulation of the AMPK/PGC-1α signaling pathway.BMC cancer · 2024Pooled it
- A Novel Autophagy InhibitorResearch (Washington, D.C.) · 2026Article
- Mitochondrial-targeted plastoquinone therapy prevents early onset muscle weakness that occurs before atrophy during ovarian cancer.Molecular metabolism · 2025Article
- Salsalate improves the anti-tumor efficacy of lenvatinib in MASH-driven hepatocellular carcinoma.JHEP reports : innovation in hepatology · 2025Article
- Rethinking AMPK: A Reversible Switch Fortifying Cancer Cell Stress-Resilience.The Yale journal of biology and medicine · 2025Review
- Small Molecule Modulators of AMP-Activated Protein Kinase (AMPK) Activity and Their Potential in Cancer Therapy.Journal of medicinal chemistry · 2025Review
- The metabolic sensor AMPK: Twelve enzymes in one.Molecular metabolism · 2024Review
- Muscle weakness and mitochondrial stress occur before severe metastasis in a novel mouse model of ovarian cancer cachexia.Molecular metabolism · 2024Article
- Muscle weakness and mitochondrial stress occur before metastasis in a novel mouse model of ovarian cancer cachexia.bioRxiv : the preprint server for biology · 2024Article
- New insights into activation and function of the AMPK.Nature reviews. Molecular cell biology · 2023Review
- Metabolic Reprogramming and Potential Therapeutic Targets in Lymphoma.International journal of molecular sciences · 2023Review
- Acetyl-CoA metabolism in cancer.Nature reviews. Cancer · 2023Review
- Muscle weakness precedes atrophy during cancer cachexia and is linked to muscle-specific mitochondrial stress.JCI insight · 2022Article
- AMPK signaling and its targeting in cancer progression and treatment.Seminars in cancer biology · 2022Review
- AMP-activated protein kinase β1 or β2 deletion enhances colon cancer cell growth and tumorigenesis.Acta biochimica et biophysica Sinica · 2022Article
- Mutant p53, the Mevalonate Pathway and the Tumor Microenvironment Regulate Tumor Response to Statin Therapy.Cancers · 2022Review
- Midkine noncanonically suppresses AMPK activation through disrupting the LKB1-STRAD-Mo25 complex.Cell death & disease · 2022Article
- p53 Is Not Required for High CIN to Induce Tumor Suppression.Molecular cancer research : MCR · 2021Article
- AMP-Activated Protein Kinase: Do We Need Activators or Inhibitors to Treat or Prevent Cancer?International journal of molecular sciences · 2020Review
- Adapt and conquer: Metabolic flexibility in cancer growth, invasion and evasion.Molecular metabolism · 2020Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The AMP-activated protein kinase (AMPK) is a heterotrimeric protein complex that is an important sensor of cellular energy status. Reduced expression of the AMPK β1 isoform has been linked to reduced survival in different cancers, but whether this accelerates tumor progression and the potential mechanism mediating these effects are not known. Furthermore, it is unknown whether AMPK β1 is implicated in tumorigenesis, and if so, what tissues may be most sensitive. In the current study, we find that in the absence of the tumor suppressor p53, germline genetic deletion of AMPK β1 accelerates the appearance of a T-cell lymphoma that reduces lifespan compared to p53 deficiency alone. This increased tumorigenesis is linked to increases in interleukin-1β (IL1β), reductions in acetyl-CoA carboxylase (ACC) phosphorylation, and elevated lipogenesis. Collectively, these data indicate that reductions in the AMPK β1 subunit accelerate the development of T-cell lymphoma, suggesting that therapies targeting this AMPK subunit or inhibiting lipogenesis may be effective for limiting the proliferation of p53-mutant tumors.
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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 Socratic graph.