ReviewCellular and molecular life sciences : CMLS2020
The enhancement of glycolysis regulates pancreatic cancer metastasis.
Review in Cellular and molecular life sciences : CMLS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05587088 (Evaluation of the Safety and Efficacy of Esperanza Extract), which is not on this map. Cited by 224 papers, 2 of them syntheses 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.
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.
Evaluation of the Safety and Efficacy of Esperanza Extract (Petiveria Alliacea) in Patients With Metastatic Gastrointestinal Tumors and Acute Leukemia
Who cites it
224 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Current hotspots and trends in cancer metabolic reprogramming: a scientometric analysis.Frontiers in immunology · 2024Pooled it
- Prognostic value of glycolysis markers in pancreatic cancer: A systematic review and meta-analysis.Frontiers in oncology · 2022Pooled it
- The regulatory roles of non-coding RNAs in aerobic glycolysis and therapeutic potential in pancreatic ductal adenocarcinoma.Annals of medicine · 2026Review
- FGD5 regulates PGK1 ubiquitination to synergize with 2-deoxy-D-glucose in pancreatic ductal adenocarcinoma.Oncogene · 2026Article
- miR-27b-5p targets RAB27A to regulate exosome secretion and migration of pancreatic cancer cells.Translational cancer research · 2026Article
- HIFs: The central drivers of tumors and their role as molecular switches in targeted therapy?Acta pharmaceutica Sinica. B · 2026Review
- S100A10 promotes glycolysis and malignant progression of CCA by activating the HK2/ERK signaling pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- Rewiring glucose metabolism in pancreatic cancer by natural compounds: implications for immune evasion and therapeutic targets.Molecular biology reports · 2026Review
- SASH1 Inhibits Gastric Cancer Progression by Regulating YAP1-Mediated Metabolic Reprogramming.Applied biochemistry and biotechnology · 2026Article
- Review
- Icariin suppresses glycolysis in prostate cancer by upregulating ALKBH5 to mediate EARS2 mJournal of molecular histology · 2026Article
- Identification of prognostic genes and development of a risk model for pancreatic cancer based on hypoxia- and lipid metabolism-related genes.Discover oncology · 2026Article
- PKM2-Mediated Glycolytic Reprogramming in Thyroid Cancer: Mechanistic Insights and Therapeutic Potential.Molecules (Basel, Switzerland) · 2026Review
- Conserved principles of central carbon partitioning in Hippo-Yorkie-drivenbioRxiv : the preprint server for biology · 2026Article
- A novel mitochondrial-associated risk score reveals a potential link between pancreatic ductal adenocarcinoma and chemotherapy resistance as well as poor response to immunotherapy.Discover oncology · 2026Article
- CDC6/THBS1 accelerates pancreatic cancer progression via AKT-mediated glycolytic reprogramming.Cell death & disease · 2026Article
- Metabolic plasticity in pancreatic ductal adenocarcinoma progression and response to treatment.Molecular cancer · 2026Review
- The histone acylation network: emerging therapeutic targets for remodeling the epigenetic landscape in pancreatic ductal adenocarcinoma.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- ANOS1 Facilitated Tumorigenesis in Gastric Cancer through the Regulation of Oxidative Phosphorylation Pathway.Journal of microbiology and biotechnology · 2026Article
- MiR-641 targets TMEFF2/MEK/PI3K to promote stem cell characteristics of pancreatic cancer cells.Discover oncology · 2026Article
164 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.
Funding
Abstract
Pancreatic ductal adenocarcinoma is prone to distant metastasis and is expected to become the second leading cause of cancer-related death. In an extremely nutrient-deficient and hypoxic environment resulting from uncontrolled growth, vascular disturbances and desmoplastic reactions, pancreatic cancer cells utilize "metabolic reprogramming" to satisfy their energy demand and support malignant behaviors such as metastasis. Notably, pancreatic cancer cells show extensive enhancement of glycolysis, including glycolytic enzyme overexpression and increased lactate production, and this is caused by mitochondrial dysfunction, cancer driver genes, specific transcription factors, a hypoxic tumor microenvironment and stromal cells, such as cancer-associated fibroblasts and tumor-associated macrophages. The metabolic switch from oxidative phosphorylation to glycolysis in pancreatic cancer cells regulates the invasion-metastasis cascade by promoting epithelial-mesenchymal transition, tumor angiogenesis and the metastatic colonization of distant organs. In addition to aerobic glycolysis, oxidative phosphorylation also plays a critical role in pancreatic cancer metastasis in ways that remain unclear. In this review, we expound on the intracellular and extracellular causes of the enhancement of glycolysis in pancreatic cancer and the strong association between glycolysis and cancer metastasis, which we expect will yield new therapeutic approaches targeting cancer metabolism.
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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.