ArticleDiscover oncology2025
Chito-oligosaccharide impairs the proliferation, invasion and migration of pancreatic cancer cells.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Promoting Wound Regeneration Through Targeted Suppression of Chronic Inflammation with Active Molecular Chitosan.Gels (Basel, Switzerland) · 2026Article
- Polysaccharide-based anticancer therapeutics: molecular mechanisms, translational advances, and the road toward precision oncology.Frontiers in pharmacology · 2026Review
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Authors and funding
5 authors.
Funding
Abstract
backgroundChito-oligosaccharide (COS) is a low molecular weight polymer obtained by degrading chitosan through special enzymatic technology, with good water solubility and high biological activity. It is also the only positively charged cationic basic amino oligosaccharide in nature. Studies have confirmed that COS has antitumour effect, but research on its effect on pancreatic cancer (PC) remains limited and unclear. This study aimed to explore the effects of COS on PC cells (PANC-1 and MIAPaCa-2).
methodWe used different concentrations of COS to treat PC cells and conducted Cell Counting Kit-8, wound-healing, and transwell assays to evaluate the proliferation, invasion, and migration ability of PC cells, respectively. Western blot was conducted to assess the expression levels of epithelial-mesenchymal transition (EMT) related markers.
resultThe proliferation, invasion, and migration ability of PC cells (PANC-1 and MIAPaCa-2) gradually decreased in a manner dependent on COS concentration. COS at 10 mg/mL exerted the strongest inhibitory effect on the two PC cell lines. At 10 mg/mL, the proliferative activity was 60.61% ± 5.25% and 64.02% ± 4.96%, respectively; the invasive ability was (18.67 ± 4.416) and (31.33 ± 3.162), respectively; and the cell-migration ability was 26.83% ± 0.442% and 17.66% ± 0.647%, respectively. The expression levels of N-cadherin and vimentin were significantly downregulated in PANC-1 cells (0.198 ± 0.047 and 0.225 ± 0.038, respectively) and MIAPaCa-2 cells (0.214 ± 0.094 and 0.214 ± 0.094, respectively) at 10 mg/mL, respectively. Conversely, E-cadherin was upregulated (0.460 ± 0.037 and 0.491 ± 0.047, respectively). Compared with control group, the differences were statistically significant.
conclusionThe upregulation of E-cadherin and the downregulation of vimentin and N-cadherin suggested that the specific mechanism of COS in PC may be related to EMT. This study provided a new direction for PC treatment.
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