P38 MAPK protects against TNF-α-provoked apoptosis in LNCaP prostatic cancer cells
Autor: | Benito Fraile, Carlos F. González Fernández, Mónica Ricote, Ignacio García-Tuñón, Patricio Aller, Ricardo Paniagua, Mar Royuela |
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Rok vydání: | 2006 |
Předmět: |
Male
Cancer Research Pyridines p38 mitogen-activated protein kinases Blotting Western Clinical Biochemistry Pharmaceutical Science Apoptosis Biology urologic and male genital diseases p38 Mitogen-Activated Protein Kinases chemistry.chemical_compound Western blot Cell Line Tumor LNCaP medicine Humans DAPI Extracellular Signal-Regulated MAP Kinases Protein Kinase Inhibitors Anthracenes Flavonoids Pharmacology Dose-Response Relationship Drug medicine.diagnostic_test Tumor Necrosis Factor-alpha Kinase Biochemistry (medical) Imidazoles JNK Mitogen-Activated Protein Kinases Prostatic Neoplasms Cell Biology chemistry Cancer cell Cancer research Tumor necrosis factor alpha Signal Transduction |
Zdroj: | Apoptosis. 11:1969-1975 |
ISSN: | 1573-675X 1360-8185 |
DOI: | 10.1007/s10495-006-0086-9 |
Popis: | Purpose: One of the most relevant aspects in cell death regulation is the signalling of apoptosis by the serine/threonine kinases MAPKs. The aim of this study was to investigate the effects of TNF-α stimulation on MAPK activation, and the pro- or anti-apoptotic role of these kinases in LNCaP and PC3 cells. Material and methods: Treatments were carried out using several TNF-α concentrations, as well as specific pharmacological inhibitors of MAPKs. Apoptosis rates were evaluated by DAPI staining and flow cytometry. MAPK phosphorylation/activation was measured by Western blot. Results: TNF-α induced apoptosis in a dose-dependent manner in LNCaP but not in PC3 cells. The MAPK inhibitors revealed that the apoptotic rate in LNCaP cells increased significantly following p38 inhibition. The kinase inhibitors failed to cause changes in apoptosis in PC3 cells. Conclusions: The potentiation of apoptosis by p38 inhibition points to this kinase as a possible target for the treatment of androgen-dependent prostatic cancer. |
Databáze: | OpenAIRE |
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