ArticleOncogene2019
Negative regulation of AMPKα1 by PIM2 promotes aerobic glycolysis and tumorigenesis in endometrial cancer.
Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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Who cites it
28 citing papers in PubMed, 46 citations in OpenAlex.
- Lactate and lactylation: mechanisms, function, diseases, and therapeutic targets.Molecular biomedicine · 2026Review
- Machine learning-based signature for prognosis and drug sensitivity in hepatocellular carcinoma using glycolysis-related gene.Oncology letters · 2026Article
- AMPK at the interface of nutrient sensing, metabolic flux and energy homeostasis.Nature metabolism · 2026Review
- Interactions between ferroptosis and tumour development mechanisms: Implications for gynaecological cancer therapy (Review).Oncology reports · 2025Review
- Mechanism of PTPN18 for regulating the migration and invasion of endometrial cancer cells via the MYC/PI3K/AKT pathway.Histology and histopathology · 2025Article
- PAK5-mediated PKM2 phosphorylation is critical for anaerobic glycolysis in endometriosis.Frontiers of medicine · 2024Article
- Phosphorylation of USP27X by PIM2 promotes glycolysis and breast cancer progression via deubiquitylation of MYC.Oncogene · 2024Article
- Identification of potential PIM-2 inhibitors via ligand-based generative models, molecular docking and molecular dynamics simulations.Molecular diversity · 2024Article
- Arginine methylation of ALKBH5 by PRMT6 promotes breast tumorigenesis via LDHA-mediated glycolysis.Frontiers of medicine · 2024Article
- Glucose metabolism reprogramming in gynecologic malignant tumors.Journal of Cancer · 2024Review
- Ferroptosis, Metabolic Rewiring, and Endometrial Cancer.International journal of molecular sciences · 2023Review
- PIM2 Promotes the Development of Ovarian Endometriosis by Enhancing Glycolysis and Fibrosis.Reproductive sciences (Thousand Oaks, Calif.) · 2023Article
- FDX1 enhances endometriosis cell cuproptosis via G6PD-mediated redox homeostasis.Apoptosis : an international journal on programmed cell death · 2023Article
- Lactate metabolism-related genes to predict the clinical outcome and molecular characteristics of endometrial cancer.BMC cancer · 2023Article
- Glucose metabolic reprogramming and its therapeutic potential in obesity-associated endometrial cancer.Journal of translational medicine · 2023Review
- Article
- PIM3-AMPK-HDAC4/5 axis restricts MuERVL-marked 2-cell-like state in embryonic stem cells.Stem cell reports · 2022Article
- Targeting PIM2 by JP11646 results in significant antitumor effects in solid tumors.International journal of oncology · 2022Article
- Phosphorylation of PFKFB4 by PIM2 promotes anaerobic glycolysis and cell proliferation in endometriosis.Cell death & disease · 2022Article
- Ubiquitination of NF-κB p65 by FBXW2 suppresses breast cancer stemness, tumorigenesis, and paclitaxel resistance.Cell death and differentiation · 2022Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endometrial cancer (EC) is one of the most common gynecologic malignancies. However, the molecular mechanisms underlying the development and progression of EC remain unclear. Here, we demonstrated that the protein proviral insertion in murine lymphomas 2 (PIM2) was necessary for maintaining EC tumorigenesis in vivo and in vitro, and could inhibit AMPKα1 kinase activity in EC cells. Specifically, we found that PIM2 bound to AMPKα1, and directly phosphorylated it on Thr467. Phosphorylation of AMPKα1 by PIM2 led to decreasing AMPKα1 kinase activity, which in turn promoted aerobic glycolysis and tumor growth. In addition, PIM2 expression positively correlated with AMPKα1 Thr467 phosphorylation in EC tissues. Further, treatment with a combination of the PIM2 inhibitor SMI-4a and the AMPKα1 activator AICAR could effectively inhibit tumor growth. Thus, our findings provide insight into the role of PIM2 and AMPKα1 in EC and suggest that combination targeting of these proteins may represent a new strategy for EC treatment.
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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.