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Updated: May 2, 2026
An Orthotopic Resectional Mouse Model of Pancreatic Cancer
Published on: September 24, 2020
Resveratrol plays dual roles in pancreatic cancer cells
Lei Yang1, Liang Yang, Wencong Tian
1Department of Histology and Embryology, Nankai University School of Medicine, 94 Weijin Road, Nankai District, Tianjin, 300071, China.
Purpose:
Although the potential anticancer effect of resveratrol (RSV) on pancreatic cancer has been reported, its mechanism was not fully understood. The role of vascular endothelial growth factor B (VEGF-B) in cancer remains controversial. Herein, we aimed to examine whether the anticancer effect of RSV was related to the VEGF-B.
Methods:
The effect of RSV on pancreatic cancer cell line (capan-2 cells) was evaluated by CCK-8 assay, Hoechst 33342 staining, and flow cytometry. The mRNA level of VEGF-B was measured by real-time PCR. VEGF-B expression was knockdown by small interfering RNA (siRNA).The protein levels of VEGF-B, glycogen synthase kinase-3 beta (GSK-3β), and Bax were measured by Western blot.
Results:
Resveratrol treatment inhibited tumor growth, induced apoptosis, and up-regulated Bax expression in capan-2 cells. The mRNA and protein levels of VEGF-B were up-regulated after RSV treatment. However, VEGF-B siRNA treatment increased the apoptotic rate, and inhibited tumor activator GSK-3β, while Bax expression was not affected. The combination of RSV and VEGF-B siRNA showed significantly higher apoptotic rate in comparison with RSV or VEGF-B siRNA mono-treatment group.
Conclusions:
Resveratrol plays dual roles in pancreatic cancer: as a tumor suppressor via the up-regulation of Bax; as a tumor activator via the up-regulation of VEGF-B; and the anticancer effect of RSV is much stronger than the cancer promotion effect. The combination of RSV with pharmacological inhibitor of VEGF-B might, therefore, be a promising modality for clinical pancreatic cancer therapy.
Insights
Resveratrol (RSV) shows anticancer effects in pancreatic cancer by up-regulating Bax, but also promotes tumor growth via VEGF-B. Combining RSV with VEGF-B inhibition enhances its therapeutic potential.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Resveratrol (RSV) exhibits potential anticancer properties, but its precise mechanisms in pancreatic cancer are not fully elucidated.
- The role of vascular endothelial growth factor B (VEGF-B) in cancer progression remains a subject of debate.
Purpose of the Study:
- To investigate the relationship between the anticancer effects of resveratrol and VEGF-B expression in pancreatic cancer cells.
- To determine if resveratrol's impact on pancreatic cancer is mediated through modulation of VEGF-B.
Main Methods:
- Cell viability was assessed using CCK-8 assay.
- Apoptosis was evaluated via Hoechst 33342 staining and flow cytometry.
- VEGF-B, GSK-3β, and Bax expression levels were quantified using real-time PCR and Western blot, with VEGF-B knockdown achieved via siRNA.
Main Results:
- Resveratrol inhibited pancreatic cancer cell growth, induced apoptosis, and increased Bax expression.
- RSV treatment led to increased mRNA and protein levels of VEGF-B.
- VEGF-B knockdown enhanced apoptosis and reduced GSK-3β, without affecting Bax; combined RSV and VEGF-B siRNA treatment yielded superior apoptotic rates.
Conclusions:
- Resveratrol exerts dual effects in pancreatic cancer, acting as a tumor suppressor through Bax upregulation and a tumor promoter via VEGF-B upregulation.
- The tumor-suppressive actions of resveratrol outweigh its tumor-promoting effects.
- Combining resveratrol with VEGF-B inhibitors presents a promising therapeutic strategy for pancreatic cancer treatment.
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