ArticleOncotarget2017
Elevation of β-galactoside α2,6-sialyltransferase 1 in a fructoseresponsive manner promotes pancreatic cancer metastasis.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 61 citations in OpenAlex.
- Sialic acids modulate immune responses in cancer: Therapeutic opportunities.The Journal of biological chemistry · 2026Review
- Enhanced sialylation of bone marrow mesenchymal stromal cells contributes to immune remodeling through macrophage polarization in multiple myeloma patients.Frontiers in immunology · 2026Article
- Fructose metabolism as an adaptive survival axis in pancreatic cancer: mechanistic insights and therapeutic implications.Frontiers in medicine · 2026Review
- Fructose Metabolism in Cancer: Molecular Mechanisms and Therapeutic Implications.International journal of medical sciences · 2025Review
- Glycosylation in Cancer.Handbook of experimental pharmacology · 2025Review
- ST6GAL1 Promotes Epithelial-to-Mesenchymal Transition in Breast Cancer via the HIF-HK2 Signaling Pathway.Breast cancer (Dove Medical Press) · 2025Article
- Development of a Novel, Potent, and Selective Sialyltransferase Inhibitor for Suppressing Cancer Metastasis.International journal of molecular sciences · 2024Article
- Lifestyle Medicine for the Prevention and Treatment of Pancreatitis and Pancreatic Cancer.Diagnostics (Basel, Switzerland) · 2024Review
- Roles of clinical application of lenvatinib and its resistance mechanism in advanced hepatocellular carcinoma (Review).American journal of cancer research · 2024Review
- Identification of significant biomarkers for predicting the risk of bipolar disorder with arteriosclerosis based on integrative bioinformatics and machine learning.Frontiers in psychiatry · 2024Article
- Fructose-Induced mTORC1 Activation Promotes Pancreatic Cancer Progression through Inhibition of Autophagy.Cancer research · 2023Article
- Role of ST6GAL1 in Thyroid Cancers: Insights from Tissue Analysis and Genomic Datasets.International journal of molecular sciences · 2023Article
- GLUT5, GLUT7, and GLUT11 expression and Bcl-2/Bax ratio on Breast Cancer Cell Line MCF-7 Treated with Fructose and Glucose.Asian Pacific journal of cancer prevention : APJCP · 2023Article
- ST6GAL1 sialyltransferase promotes acinar to ductal metaplasia and pancreatic cancer progression.JCI insight · 2023Article
- The Role of Paxillin Aberrant Expression in Cancer and Its Potential as a Target for Cancer Therapy.International journal of molecular sciences · 2023Review
- Histopathologic and proteogenomic heterogeneity reveals features of clear cell renal cell carcinoma aggressiveness.Cancer cell · 2023Article
- Role of tumor cell sialylation in pancreatic cancer progression.Advances in cancer research · 2023Review
- Sialyltransferases and Neuraminidases: Potential Targets for Cancer Treatment.Diseases (Basel, Switzerland) · 2022Review
- Extracellular sialyltransferase st6gal1 in breast tumor cell growth and invasiveness.Cancer gene therapy · 2022Article
- Review
Corrections and comments
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Authors and funding
15 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive type of pancreatic cancer with clinical characteristics of local invasion and early metastasis. Recent cohort studies indicate high fructose intake is associated with an increase in pancreatic cancer risk. However, the mechanisms by which fructose promotes pancreatic tumorigenesis remain unclear. Herein, Kras+/LSLG12D mice were crossed with Elas-CreER transgenic mice to determine whether fructose intake directly contributes to tumor formation. Orthotopic tumor-xenograft experiments were performed to determine whether fructose substitution enhances the metastatic potential of PDAC cells. The mechanisms underlying the effects of fructose were explored by RNAseq analysis in combination with high-performance anion exchange chromatography. Dietary fructose was initially found to promote the development of aggressive pancreatic cancer in mice conditionally expressing KrasG12D in the adult pancreas. We further revealed that fructose substitution enhanced the metastatic potential of human PDAC cell via selective outgrowth of aggressive ABCG2-positive subpopulations and elevating N-acetylmannosamine levels that upregulated β-galactoside α2,6-sialyltransferase 1 (ST6Gal1), thereby promoting distant metastasis. Finally, we observed that PDAC patients expressing higher levels of ST6Gal1 and GLUT5 presented poorer prognosis compared to other groups. In conclusion, our findings have elucidated a crucial role of ST6Gal1 in regulating the invasiveness of PDACs in a fructose-responsive manner.
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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.