P38 MAPK protects against TNF-α-provoked apoptosis in LNCaP prostatic cancer cells
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.
KeywordsApoptosis Protate Cancer LNCap PC3 P38 TNF
Unable to display preview. Download preview PDF.
- 10.De Miguel MP, Royuela M, Bethencourt FR, Santamaria L, Fraile B, Paniagua R (2000) Immunoexpression of tumour necrosis factor-alpha and its receptors 1 and 2 correlates with proliferation/apoptosis equilibrium in normal, hyperplasic and carcinomatous human prostate. Cytokine 12:535–538PubMedCrossRefGoogle Scholar