Regulation of growth of prostate cancer cells selected in the presence of interleukin-6 by the anti-interleukin-6 antibody CNTO 328
| Autor: | Hannes Steiner, Alfred Hobisch, Jeffrey A. Nemeth, Zoran Culig, Hermann Dietrich, Patrizia Moser, Marian T. Nakada, Ilaria T. Cavarretta, Mohamed H. Zaki, Jasmin Bektic, Andreas P. Berger |
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| Rok vydání: | 2006 |
| Předmět: |
Male
STAT3 Transcription Factor Vascular Endothelial Growth Factor A medicine.medical_specialty Urology medicine.medical_treatment Mice Nude Cell Growth Processes Mice chemistry.chemical_compound Prostate cancer Cell Line Tumor Internal medicine Animals Humans Medicine Viability assay Phosphorylation Interleukin 6 Mitogen-Activated Protein Kinase 1 Mitogen-Activated Protein Kinase 3 Transglutaminases biology Interleukin-6 business.industry Kinase Antibodies Monoclonal Prostatic Neoplasms medicine.disease Xenograft Model Antitumor Assays Vascular endothelial growth factor Ki-67 Antigen Cytokine Endocrinology Proto-Oncogene Proteins c-bcl-2 Oncology chemistry biology.protein Cancer research Immunohistochemistry Antibody business |
| Zdroj: | The Prostate. 66:1744-1752 |
| ISSN: | 1097-0045 0270-4137 |
| Popis: | BACKGROUND Interleukin-6 (IL-6) is a multifunctional regulator of cellular events in prostate cancer. LNCaP-IL-6+ cells selected in the presence of IL-6 were taken for assessment of effects of the chimeric monoclonal anti-IL-6 antibody CNTO 328. METHODS Cell viability was assessed after treatment with CNTO 328 by the ATP assay. Expression of Bcl-2 and Bax and activation of signaling pathways were evaluated by Western analysis. Nude mice were inoculated with LNCaP-IL-6+ cells and treated with CNTO 328. The tumors were analyzed by immunohistochemistry for expression of Ki-67, tissue transglutaminase, and vascular endothelial growth factor. RESULTS CNTO 328 caused a statistically significant inhibition of cell viability. The protein levels of Bcl-2 and the phosphorylation of ERK1/2 mitogen-activated protein kinases were decreased by the anti-IL-6 antibody. Treatment with CNTO 328 yielded an increase in the phosphorylation of signal transducers and activators of transcription factor 3. The mean tumor volume in animals inoculated with LNCaP-IL-6+ cells and treated with CNTO 328 was insignificantly lower than that in animals treated with the control antibody. There was a statistically significant decrease in the percentage of Ki-67-positive cells in CNTO 328-treated tumors. CONCLUSION CNTO 328 has a potential in prostate cancer therapy and could be further tested in various combination experimental treatments. Prostate © 2006 Wiley-Liss, Inc. |
| Databáze: | OpenAIRE |
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