Abstract | BACKGROUND: 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.
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Authors | A Yu, P Somasundar, A Balsubramaniam, A T Rose, L Vona-Davis, D W McFadden |
Journal | The Journal of surgical research
(J Surg Res)
Vol. 105
Issue 1
Pg. 65-8
(Jun 01 2002)
ISSN: 0022-4804 [Print] United States |
PMID | 12069504
(Publication Type: Journal Article)
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Copyright | (c) 2002 Elsevier Science (USA). |
Chemical References |
- Antineoplastic Agents
- Antioxidants
- Endothelial Growth Factors
- Lymphokines
- Receptors, Neuropeptide Y
- Vascular Endothelial Growth Factor A
- Vascular Endothelial Growth Factors
- Peptide YY
- Vitamin E
- neuropeptide Y4 receptor
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Topics |
- Antineoplastic Agents
(pharmacology)
- Antioxidants
(pharmacology)
- Cell Division
(drug effects)
- Endothelial Growth Factors
(biosynthesis)
- Humans
- Lymphokines
(biosynthesis)
- Male
- Peptide YY
(pharmacology)
- Prostatic Neoplasms
- Receptors, Neuropeptide Y
(agonists)
- Tumor Cells, Cultured
(cytology, drug effects, metabolism)
- Vascular Endothelial Growth Factor A
- Vascular Endothelial Growth Factors
- Vitamin E
(pharmacology)
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