ArticleCancer research2020
p38γ MAPK Is Essential for Aerobic Glycolysis and Pancreatic Tumorigenesis.
Article in Cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. It is linked to trial NCT05132244 (Pancreatic Cancer Glucose Assessment and Regulation Study), which is not on this map. Cited by 53 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.
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.
Pancreatic Cancer Glucose Assessment and Regulation Study
Who cites it
53 citing papers in PubMed, 79 citations in OpenAlex.
- The regulatory roles of non-coding RNAs in aerobic glycolysis and therapeutic potential in pancreatic ductal adenocarcinoma.Annals of medicine · 2026Review
- p38γ and p38δ MAP kinases in inflammation.Biochemical Society transactions · 2026Review
- Review
- P38γ drives aerobic glycolysis in liver sinusoidal endothelial cells and regulates alcoholic liver disease via the PFKFB3 signaling pathway.Molecular biology reports · 2026Article
- CSDE1 Drives Glycolysis and the Progression of Prostate Cancer Through RAC1-Dependent RAS/MAPK Activation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Solute Carrier transporters in tumor metabolism and immune modulation: implications for therapy.Journal of translational medicine · 2026Review
- Metabolic Vulnerabilities as a Therapeutic Target in Breast Cancer.Current oncology (Toronto, Ont.) · 2026Review
- Energy Metabolism and Cancer Pain: A Pathway to Innovative Treatment Strategies.Current topics in medicinal chemistry · 2026Review
- Enhancement of melanoma aggressiveness via p38-MAPK, HIF-1α pathways, and metabolic reprogramming induced by Candida albicans.Scientific reports · 2025Article
- Tumor glucose reprogramming suppresses cuproptosis: A review.Biomolecules & biomedicine · 2025Review
- UHRF1-mediated epigenetic reprogramming regulates glycolysis to promote progression of B-cell acute lymphoblastic leukemia.Cell death & disease · 2025Article
- S100A2 promotes clear cell renal cell carcinoma tumor metastasis through regulating GLUT2 expression.Cell death & disease · 2025Article
- Enhanced Antitumor Activity of Korean Black Soybean Cultivar 'Soman' by Targeting STAT-Mediated Aerobic Glycolysis.Antioxidants (Basel, Switzerland) · 2025Article
- The Novel Prognostic Biomarker MAPK12 Promotes Migration, Proliferation, and Invasion in Head and Neck Squamous Cell Carcinoma.Current medicinal chemistry · 2025Article
- Reprogramming of glucose metabolism in pancreatic cancer: mechanisms, implications, and therapeutic perspectives.Frontiers in immunology · 2025Review
- Pan-Immune-Inflammation Value (PIV) and Prognostic Nutritional Index (PNI) are Associated with Distant Metastasis in Colorectal Cancer withInternational journal of general medicine · 2025Article
- Ubiquitin-specific protease 7 maintains c-Myc stability to support pancreatic cancer glycolysis and tumor growth.Journal of translational medicine · 2024Article
- Article
- A retrospective analysis of the clinicopathological features and prognostic value of MAPK12 protein expression in diffuse large B-cell lymphoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024Article
- SPARC activates p38γ signaling to promote PFKFB3 protein stabilization and contributes to keloid fibroblast glycolysis.Inflammation and regeneration · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
17 authors at 3 institutions in 3 countries.
Funding
Abstract
KRAS is mutated in most pancreatic ductal adenocarcinomas (PDAC) and yet remains undruggable. Here, we report that p38γ MAPK, which promotes PDAC tumorigenesis by linking KRAS signaling and aerobic glycolysis (also called the Warburg effect), is a novel therapeutic target. p38γ interacted with a glycolytic activator PFKFB3 that was dependent on mutated KRAS. KRAS transformation and overexpression of p38γ increased expression of PFKFB3 and glucose transporter GLUT2, conversely, silencing mutant KRAS, and p38γ decreased PFKFB3 and GLUT2 expression. p38γ phosphorylated PFKFB3 at S467, stabilized PFKFB3, and promoted their interaction with GLUT2. Pancreatic knockout of p38γ decreased p-PFKFB3/PFKFB3/GLUT2 protein levels, reduced aerobic glycolysis, and inhibited PDAC tumorigenesis in KPC mice. PFKFB3 and GLUT2 depended on p38γ to stimulate glycolysis and PDAC growth and p38γ required PFKFB3/S467 to promote these activities. A p38γ inhibitor cooperated with a PFKFB3 inhibitor to blunt aerobic glycolysis and PDAC growth, which was dependent on p38γ. Moreover, overexpression of p38γ, p-PFKFB3, PFKFB3, and GLUT2 in PDAC predicted poor clinical prognosis. These results indicate that p38γ links KRAS oncogene signaling and aerobic glycolysis to promote pancreatic tumorigenesis through PFKFB3 and GLUT2, and that p38γ and PFKFB3 may be targeted for therapeutic intervention in PDAC. SIGNIFICANCE: These findings show that p38γ links KRAS oncogene signaling and the Warburg effect through PFKBF3 and Glut2 to promote pancreatic tumorigenesis, which can be disrupted via inhibition of p38γ and PFKFB3.
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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.