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Corn silk crude polysaccharide exerts anti-pancreatic cancer activity by blocking the EGFR/PI3K/AKT/CREB signaling
Hong Tao1, Xia Chen, Zhenyun Du
1Glycochemistry & Glycobiology Lab, Key Laboratory of Receptor Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China. dingkan@simm.ac.cn.
Abstract:
Pancreatic cancer is a highly lethal and malignant solid tumor. Treatments for pancreatic cancer are seriously limited because it is highly drug-resistant and immunosuppressive. Hence, it is urgent to explore novel approaches for anti-pancreatic cancer therapy. In this study, we show that S1, a crude polysaccharide from corn silk, may significantly inhibit pancreatic cancer cell proliferation in vitro and in vivo. Further studies reveal that S1 can induce pancreatic cancer cell apoptosis, arrest the cell cycle in S phase and impede pancreatic cancer cell migration and invasion. Moreover, S1 may block the EGFR/PI3K/AKT/CREB signaling pathway to exert its anti-pancreatic cancer activity. However, S1 has almost no toxicity either in vitro or in vivo. These results provide evidence that S1 is a new functional food component that can be developed to fight pancreatic cancer.
Insights
Corn silk polysaccharide S1 shows potential as a novel pancreatic cancer therapy. This compound inhibits cancer cell growth, induces apoptosis, and blocks key signaling pathways with minimal toxicity.
Area of Science:
- Oncology
- Pharmacology
- Natural Products
Background:
- Pancreatic cancer is a lethal malignancy with limited treatment options due to drug resistance and immunosuppression.
- Novel therapeutic strategies are urgently needed to combat pancreatic cancer.
- Corn silk polysaccharide S1 is investigated as a potential anti-cancer agent.
Purpose of the Study:
- To evaluate the anti-pancreatic cancer efficacy of S1, a crude polysaccharide from corn silk.
- To investigate the mechanisms underlying S1's anti-cancer activity.
- To assess the safety profile of S1 in vitro and in vivo.
Main Methods:
- In vitro and in vivo studies were conducted using pancreatic cancer models.
- Cell proliferation, apoptosis, cell cycle, migration, and invasion assays were performed.
- The effect of S1 on the EGFR/PI3K/AKT/CREB signaling pathway was analyzed.
- Toxicity assessments were carried out.
Main Results:
- S1 significantly inhibited pancreatic cancer cell proliferation in vitro and in vivo.
- S1 induced apoptosis and arrested the cell cycle in the S phase.
- S1 impeded pancreatic cancer cell migration and invasion.
- S1 blocked the EGFR/PI3K/AKT/CREB signaling pathway.
- S1 exhibited minimal toxicity.
Conclusions:
- S1 demonstrates significant anti-pancreatic cancer activity.
- S1 functions by inducing apoptosis, cell cycle arrest, and inhibiting migration/invasion, potentially via the EGFR/PI3K/AKT/CREB pathway.
- S1 is a promising functional food component for pancreatic cancer therapy with a favorable safety profile.
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