Critical role of the c-JunNH2-terminal kinase and p38 mitogen-activated protein kinase pathways on sodium butyrate-induced apoptosis in DU145 human prostate cancer cells

Cho, SD; Ahn, NS; Jung, JW; Yang, SR; Park, JS; Lee, YS; Jo, EH; Hwang, JW; Lii, J; Kang, KS

HERO ID

1298601

Reference Type

Journal Article

Year

2006

Language

English

PMID

16374231

HERO ID 1298601
In Press No
Year 2006
Title Critical role of the c-JunNH2-terminal kinase and p38 mitogen-activated protein kinase pathways on sodium butyrate-induced apoptosis in DU145 human prostate cancer cells
Authors Cho, SD; Ahn, NS; Jung, JW; Yang, SR; Park, JS; Lee, YS; Jo, EH; Hwang, JW; Lii, J; Kang, KS
Journal European Journal of Cancer Prevention
Volume 15
Issue 1
Page Numbers 57-63
Abstract Sodium butyrate (NaBu) is known to exhibit anti-cancer effects via the differentiation and apoptosis of various carcinoma cells. However, the mechanism by which NaBu induces apoptosis and the involvement of protein kinases during apoptosis is not completely understood. To investigate the underlying pathways, we performed cell culture experiments in androgen-independent human prostate cancer (DU145 cells) focusing on various protein kinases. NaBu causes concentration-dependent cell detachment and growth inhibition. Exposure of DU145 cells to NaBu for 24 h caused a strong apoptotic effect with 26% nuclear fragmentation and condensation. In addition, NaBu induced caspase-3 and poly-ADP ribose polymerase cleavage and up-regulation of bax, suggesting that mitochondrial damage is involved in NaBu-induced caspase-dependent apoptosis. Interestingly, NaBu stimulated p38 mitogen-activated protein kinase (MAPK) and c-Jun NH2-terminal kinase (JNK) activation, but not extracellular signal-regulated kinase 1/2 activation during apoptosis. Furthermore, NaBu up-regulated total protein levels and phospho forms of MAPK kinase 3 (MKK3) and MAPK kinase 4 (MKK4) as the upstream kinases of p38 MAPK and JNK independently of oxidative stress. Taken together, it is suggested that NaBu can be a promising chemopreventive agent for prostate cancer and the p38 MAPK and JNK pathways have critical roles in NaBu-induced apoptosis in DU145 cells.
Pmid 16374231
Wosid WOS:000234577700009
Is Certified Translation No
Dupe Override No
Comments Source: Web of Science WOS:000234577700009
Is Public Yes
Language Text English
Keyword sodium butyrate; prostate cancer; c-Jun NH2-terminal kinase; p38 mitogen-activated protein kinase K; apoptosis