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Updated: Jul 31, 2026

A Simple Bioassay for the Evaluation of Vascular Endothelial Growth Factors
Published on: March 15, 2016
Vitamin E and the Y4 agonist BA-129 decrease prostate cancer growth and production of vascular endothelial growth
A Yu1, P Somasundar, A Balsubramaniam
1Department of Surgery, Robert C. Byrd Health Sciences Center, Morgantown, West Virginia 26506-9238, USA.
Background:
A biologically active form of vitamin E, alpha-tocopherol succinate (ATS), has been shown to induce apoptosis of hormone-refractory prostate cancer in vitro and inhibit cell growth in vivo. The gastrointestinal hormone peptide YY (PYY) has growth inhibitory activity against multiple cancer cell lines and is synergistic with ATS against breast and pancreatic cancer growth. BA-129, a specific Y4 receptor agonist, has growth inhibitory effects on pancreatic cancer in vitro. We investigated the effects of BA-129 and ATS on prostate cancer growth and evaluated their effects on vascular endothelial growth factor (VEGF) production.
Methods:
A hormone-refractory human prostate cancer cell line, PC-3, was treated with ATS alone at 10 pg/ml, PYY or BA-129 alone at doses of 75 and 500 pmol/ml, or a combination of the two agents. Cell growth was measured by MTT assay and hemocytometry using trypan blue. Quantitative measurement of VEGF was performed by ELISA. Statistical analysis was achieved by ANOVA.
Results:
ATS exhibited significant (P < 0.05) growth inhibitory effects in prostate cancer cells. PYY also inhibited growth (P < 0.05). ATS treatment reduced VEGF production (P < 0.05). PYY treatment increased VEGF. When ATS was given in combination with BA-129, VEGF production was further reduced (P < 0.05).
Conclusions:
Both PYY and ATS inhibit growth in hormone-refractory prostate cancer, with augmentation when used in combination. VEGF production is inhibited by vitamin E, but increased by PYY. ATS abolishes the augmented VEGF response to PYY. Our data suggest that PYY is involved in the regulation of VEGF production and prostate cancer growth.
Insights
Alpha-tocopherol succinate (ATS) and peptide YY (PYY) inhibit hormone-refractory prostate cancer growth. ATS reduces vascular endothelial growth factor (VEGF) production, while PYY increases it, an effect abolished by ATS in combination therapy.
Area of Science:
- Oncology
- Molecular Biology
- Endocrinology
Background:
- Alpha-tocopherol succinate (ATS), a vitamin E form, induces apoptosis and inhibits hormone-refractory prostate cancer (PCa) growth.
- Peptide YY (PYY) exhibits anti-cancer properties and synergizes with ATS in inhibiting breast and pancreatic cancer.
- BA-129, a Y4 receptor agonist, shows growth inhibitory effects on pancreatic cancer.
Purpose of the Study:
- To investigate the effects of BA-129 and ATS on hormone-refractory prostate cancer growth.
- To evaluate the impact of BA-129 and ATS on vascular endothelial growth factor (VEGF) production in prostate cancer.
Main Methods:
- PC-3 human prostate cancer cells were treated with ATS, PYY, or BA-129 alone or in combination.
- Cell growth was assessed using MTT assay and hemocytometry (trypan blue exclusion).
- VEGF levels were quantified by ELISA; statistical significance was determined by ANOVA.
Main Results:
- Both ATS and PYY demonstrated significant growth inhibition in PC-3 cells.
- ATS treatment decreased VEGF production, whereas PYY treatment increased it.
- Combination therapy with ATS and BA-129 further reduced VEGF production.
Conclusions:
- PYY and ATS synergistically inhibit hormone-refractory prostate cancer growth.
- ATS inhibits VEGF production, while PYY augments it; ATS counteracts PYY's effect on VEGF.
- PYY plays a role in regulating prostate cancer growth and VEGF production.
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