ArticleCell death & disease2024
LIN28B induced PCAT5 promotes endometrial cancer progression and glycolysis via IGF2BP3 deubiquitination.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 9 citations in OpenAlex.
- MKRN2-Mediated Degradation of IGF2BP3 Suppresses MYC and Enhances CDK4/6 Inhibitor Sensitivity in Bladder Cancer.Cancers · 2026Article
- IGF2BP3 promotes glycolysis of osteosarcoma stem cells by reading RNA m⁶A to stabilize ENO1 and promote malignant biological behavior of osteosarcoma.Cell biology and toxicology · 2026Article
- IGF2BP3 in Multi-System Diseases: Molecular Mechanisms, Pathological Roles and Translational Insights.Cell biochemistry and biophysics · 2026Review
- Lactate and lactylation: mechanisms, function, diseases, and therapeutic targets.Molecular biomedicine · 2026Review
- USP5 inhibition stimulates immunogenic ferroptosis that enhances immunotherapy in diffuse large B-cell lymphoma.Cell communication and signaling : CCS · 2026Article
- METTL3-IGF2BP3 as a glucose sensor in hyperglycemic microenvironment promotes tumorigenesis and glycolysis.International journal of biological sciences · 2026Article
- LL22NC03-N14H11.1 regulates the m6A modification of MYC and promotes glycolytic activity in hepatocellular carcinoma cells by inhibiting IGF2BP3 ubiquitination degradation.Journal of experimental & clinical cancer research : CR · 2025Article
- Molecular mechanisms by which C1orf112 promotes endometrial cancer progression and the development and validation of a clinical scoring model.Clinical epigenetics · 2025Article
- Comprehensive analysis of ceRNA Networks in UCEC: Prognostic and therapeutic implications.PloS one · 2025Article
- LIN28B promotes the progression of endometrial cancer through upregulating MYC and correlates with immune microenvironment.Frontiers in oncology · 2025Article
- Mitochondria-related genes as prognostic signature of endometrial cancer and the effect of MACC1 on tumor cells.PloS one · 2025Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endometrial cancer (EC) cells exhibit abnormal glucose metabolism, characterized by increased aerobic glycolysis and decreased oxidative phosphorylation. Targeting cellular glucose metabolism in these cells could be an effective therapeutic approach for EC. This study aimed to assess the roles of LIN28B, PCAT5, and IGF2BP3 in the glucose metabolism, proliferation, migration, and invasion of EC cells. LIN28B highly expressed in EC, binds and stabilizes PCAT5. PCAT5, overexpressed in EC, and its 1485-2288nt region can bind to the KH1-2 domain of IGF2BP3 to prevent MKRN2 from binding to the K294 ubiquitination site of IGF2BP3, thus stabilizing IGF2BP3. Finally, IGF2BP3 promotes the aerobic glycolysis, proliferation, migration and invasion of EC cells by stabilizing the key enzymes of glucose metabolism HK2 and PKM2. Taken together, our data reveal that the LIN28B/PCAT5/IGF2BP3 axis is critical for glucose reprogramming and malignant biological behavior in EC cells. Therefore, targeting this axis may contribute to the development of a novel therapeutic strategy for EC metabolism.
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