ArticlePloS one2014
Pancreatic cancer cell glycosylation regulates cell adhesion and invasion through the modulation of α2β1 integrin and E-cadherin function.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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36 citing papers in PubMed, 66 citations in OpenAlex.
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- The Research Progress of Metformin Regulation of Metabolic Reprogramming in Malignant Tumors.Pharmaceutical research · 2024Review
- Mass spectrometry analysis of intact proteinJournal of Zhejiang University. Science. B · 2024Article
- GLT8D2 is a prognostic biomarker and regulator of immune cell infiltration in gastric cancer.Frontiers in immunology · 2024Article
- Nucleotide sugar transporter SLC35A2 is involved in promoting hepatocellular carcinoma metastasis by regulating cellular glycosylation.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- Role of tumor cell sialylation in pancreatic cancer progression.Advances in cancer research · 2023Review
- Sialyltransferase Inhibitor AcCancers · 2022Article
- Altered glycosylation in pancreatic cancer and beyond.The Journal of experimental medicine · 2022Review
- Review
- Whole-Genome Analysis of De Novo Somatic Point Mutations Reveals Novel Mutational Biomarkers in Pancreatic Cancer.Cancers · 2021Article
- Role of glycosylation in TGF-β signaling and epithelial-to-mesenchymal transition in cancer.Protein & cell · 2021Review
- Altered Actin Dynamics in Cell Migration of GNE Mutant Cells.Frontiers in cell and developmental biology · 2021Article
- Altered glycosylation in cancer: A promising target for biomarkers and therapeutics.Biochimica et biophysica acta. Reviews on cancer · 2021Review
- The Adverse Impact of Tumor Microenvironment on NK-Cell.Frontiers in immunology · 2021Review
- RAGE Up-Regulation Differently Affects Cell Proliferation and Migration in Pancreatic Cancer Cells.International journal of molecular sciences · 2020Article
- Knockdown of α2,3-Sialyltransferases Impairs Pancreatic Cancer Cell Migration, Invasion and E-selectin-Dependent Adhesion.International journal of molecular sciences · 2020Article
- HLA-B influences integrin beta-1 expression and pancreatic cancer cell migration.Experimental cell research · 2020Article
- Insight in Adhesion Protein Sialylation and Microgravity Dependent Cell Adhesion-An Omics Network Approach.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In our previous studies we have described that ST3Gal III transfected pancreatic adenocarcinoma Capan-1 and MDAPanc-28 cells show increased membrane expression levels of sialyl-Lewis x (SLe(x)) along with a concomitant decrease in α2,6-sialic acid compared to control cells. Here we have addressed the role of this glycosylation pattern in the functional properties of two glycoproteins involved in the processes of cancer cell invasion and migration, α2β1 integrin, the main receptor for type 1 collagen, and E-cadherin, responsible for cell-cell contacts and whose deregulation determines cell invasive capabilities. Our results demonstrate that ST3Gal III transfectants showed reduced cell-cell aggregation and increased invasive capacities. ST3Gal III transfected Capan-1 cells exhibited higher SLe(x) and lower α2,6-sialic acid content on the glycans of their α2β1 integrin molecules. As a consequence, higher phosphorylation of focal adhesion kinase tyrosine 397, which is recognized as one of the first steps of integrin-derived signaling pathways, was observed in these cells upon adhesion to type 1 collagen. This molecular mechanism underlies the increased migration through collagen of these cells. In addition, the pancreatic adenocarcinoma cell lines as well as human pancreatic tumor tissues showed colocalization of SLe(x) and E-cadherin, which was higher in the ST3Gal III transfectants. In conclusion, changes in the sialylation pattern of α2β1 integrin and E-cadherin appear to influence the functional role of these two glycoproteins supporting the role of these glycans as an underlying mechanism regulating pancreatic cancer cell adhesion and invasion.
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