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[Suppression of VEGF protein expression by arctigenin in oral squamous cell carcinoma]
Guang-rui Pu1, Fa-yu Liu, Bo Wang
1Department of Dentistry, The First Affiliated Hospital of Dalian Medical University. Dalian 116011;China.E-mail:dl_pugr@126.com.
Purpose:
To observe arctigenin's inhibitory effect on oral squamous cell carcinoma, and explore the possible mechanism.
Methods:
The expression of VEGF in 32 cases of oral squamous cell cancer and 20 adjacent tissue specimen were detected with immunohistochemistry. Human nude mouse transplantation tumor model of oral squamous cell cancer was prepared with HSC-3 cells line. Transplanted tumor growth and VEGF expression in transplanted tumor tissues were assayed after treatment with arctigenin. One-way ANOVA was used for comparison between groups with SPSS 16.0 software package.
Results:
Compared with the adjacent tissue, immunohistochemical staining score of VEGF was significantly higher (P<0.01) in oral squamous cell carcinoma tissues. After treatment with arctigenin, the growth of oral squamous cell transplanted tumors in nude mouse was inhibited (P<0.05), and decreased weight in end point of observation was noted (P<0.05). There were significant differences between high dose group and low dose group (P<0.05). Compared with the nude mouse model group, the optical density of VEGF staining was significantly lower in arctigenin group (P<0.05). There were significant differences between high dose group and low dose group (P<0.05).
Conclusions:
Arctigenin can dose-dependently inhibit the growth of oral squamous cell carcinomas, and this effect may be related to down regulation of VEGF expression.
Insights
Arctigenin effectively inhibits oral squamous cell carcinoma growth in a dose-dependent manner. This anticancer effect is linked to the down-regulation of vascular endothelial growth factor (VEGF) expression.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Oral squamous cell carcinoma (OSCC) is a prevalent malignancy.
- Vascular Endothelial Growth Factor (VEGF) is implicated in tumor progression.
Purpose of the Study:
- To investigate the inhibitory effects of arctigenin on OSCC.
- To explore the underlying mechanisms, specifically focusing on VEGF expression.
Main Methods:
- Immunohistochemistry was used to assess VEGF expression in OSCC tissues and adjacent normal tissues.
- A human nude mouse xenograft model of OSCC was established and treated with varying doses of arctigenin.
- Tumor growth, weight, and VEGF expression in transplanted tumors were analyzed.
Main Results:
- VEGF expression was significantly higher in OSCC tissues compared to adjacent tissues.
- Arctigenin treatment significantly inhibited the growth and reduced the weight of OSCC xenografts in a dose-dependent manner.
- Arctigenin treatment led to a significant down-regulation of VEGF expression in the transplanted tumors.
Conclusions:
- Arctigenin exhibits a dose-dependent inhibitory effect on oral squamous cell carcinoma growth.
- The anticancer activity of arctigenin may be mediated through the down-regulation of VEGF expression.
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