ArticleJournal of cellular and molecular medicine2017
Up-regulation of glycolysis promotes the stemness and EMT phenotypes in gemcitabine-resistant pancreatic cancer cells.
Article in Journal of cellular and molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.
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Who cites it
99 citing papers in PubMed, 160 citations in OpenAlex.
- The regulatory roles of non-coding RNAs in aerobic glycolysis and therapeutic potential in pancreatic ductal adenocarcinoma.Annals of medicine · 2026Review
- Mep1a Knockout Attenuates Unilateral Ureteral Obstruction-Induced Renal Injury by Inhibiting Glycolysis.Current medical science · 2026Article
- SUMOylated Reptin maintains low intracellular ROS levels by activating mitophagy to drive gemcitabine resistance in gallbladder cancer.Cell death & disease · 2026Article
- The Redox Paradox of Natural Supplements in Cancer: A Narrative Review to Guide Clinical Practice.Antioxidants (Basel, Switzerland) · 2026Review
- SLPI/FBW7/c-Myc Axis Reduces Gemcitabine Sensitivity in PDAC by Enhancing Glycolysis and Impairing NK Cell Immunity.Cancer science · 2026Article
- Targeting tumor dormancy: the next frontier in gastrointestinal stromal tumor therapy.Neoplasia (New York, N.Y.) · 2026Review
- Integrated single-cell and bulk transcriptomics reveals an IGF2BP3-driven metabolic circuitry in endometrial cancer.BMC cancer · 2026Article
- Matrix stiffness induces CaExperimental hematology & oncology · 2026Article
- Plasma-Derived Extracellular Vesicles Inhibit Lipopolysaccharide-Induced Apoptosis and Oxidative Stress in Human AC16 Cardiomyocytes.Current issues in molecular biology · 2026Article
- Alpha-enolase influences ATP pool of cytoplasm and lactate homeostasis by regulating glycolysis in gastric cancer.Signal transduction and targeted therapy · 2025Article
- Proteomic Characterization of Primary Human Pancreatic Cancer Cell Lines Following Long-Term Exposure to Gemcitabine.Proteomes · 2025Article
- Lipid metabolism in cancer stem cells: reprogramming, mechanisms, crosstalk, and therapeutic approaches.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Metabolic reprogramming and prognostic insights in molecular landscapes driven by glycolysis in ovarian cancer.Scientific reports · 2025Article
- CDCA7 enhances STAT3 transcriptional activity to regulate aerobic glycolysis and promote pancreatic cancer progression and gemcitabine resistance.Cell death & disease · 2025Article
- Exploring the potential of gemcitabine-metal-organic frameworks in combating pancreatic cancer under ketogenic conditions.BMC cancer · 2025Article
- Molecular Mechanisms of Gemcitabine Resistance in Cholangiocarcinoma.Oncology research · 2025Review
- Review
- DCLK1 mediated cooperative acceleration of EMT by avian leukosis virus subgroup J and Marek's disease virus via the Wnt/β-catenin pathway promotes tumor metastasis.Journal of virology · 2024Article
- RHOF promotes Snail1 lactylation by enhancing PKM2-mediated glycolysis to induce pancreatic cancer cell endothelial-mesenchymal transition.Cancer & metabolism · 2024Article
- Review
39 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer stem cells (CSCs) and epithelial-mesenchymal transition (EMT)-type cells are considered as underlying causes of chemoresistance, tumour recurrence and metastasis in pancreatic cancer. We aimed to describe the mechanisms - particularly glycolysis - involved in the regulation of the CSC and EMT phenotypes. We used a gemcitabine-resistant (GR) Patu8988 cell line, which exhibited clear CSC and EMT phenotypes and showed reliance on glycolysis. Inhibition of glycolysis using 2-deoxy-D-glucose (2-DG) significantly enhanced the cytotoxicity of gemcitabine and inhibited the CSC and EMT phenotypes in GR cells both in vitro and in vivo. Intriguingly, the use of the reactive oxygen species (ROS) scavenger N-acetylcysteine (NAC) restored the CSC and EMT phenotypes. H
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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.