| Title | Butyrate stimulated H2S production in colon cancer cell. | | Author(s) | Cao Q, Zhang L, Yang G, Xu C, Wang R | | Institution | Lakehead University, Department of Biology, Thunder Bay, Ontario, Canada; cqhdoc@126.com. | | Source | Antioxid Redox Signal 2009 Oct 5. | | Abstract | Butyrate is a short chain fatty acid which arrests growth of various types of cells. H2S can be endogenously produced by cystathionine -lyase (CSE) and/or cystathionine beta-synthase (CBS) in colonic tissues. In the present study, we observed endogenous H2S production in a colon cancer cell line (WiDr) and colonic tissues through the activity of both CSE and CBS. After 24 h of incubation of WiDr cells, butyrate increased cell production of H2S and upregulated CBS and CSE expressions. Both butyrate and NaHS (a H2S donor) decreased cell viability in a dose-dependent manner. Blockade of CBS, but not CSE, decreased butyrate-stimulated H2S production and reversed butyrate-inhibited cell viability. In addition, NaHS treatment stimulated the phosphorylation of extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK), but not c-Jun N-terminal kinase (JNK). Inhibition of the phosphorylation of either p38 MAPK or ERK did not abolish NaHS-induced cell death. Butyrate treatment increased the phosphorylation of ERK, not p38 MAPK and JNK, but inhibition of ERK and p38 MAPK phosphorylation did not affect butyrate-reduced cell viability. In conclusion, butyrate regulates endogenous H2S production by stimulating CBS expression in colon cancer cells, but butyrate and H2S inhibit cancer cell growth through different mechanisms. | | Language | ENG | | Pub Type(s) | JOURNAL ARTICLE
| | PubMed ID | 19803745 |
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