Dietary Sphingomyelin Inhibits Colonic Tumorigenesis with an Up-regulation of Alkaline Sphingomyelinase Expression in ICR Mice
(2008) In Anticancer research 28(6A). p.3631-3635- Abstract
- Background: Sphingomyelin (SM) hydrolysis generates biologically active products regulating cell growth, differentiation and apoptosis. Dietary SM has been found to inhibit colonic tumorigenesis. Alkaline sphingomyelinase (alk-SMase) is the key enzyme responsible for sphingomyelin digestion in the gut. Whether or not dietary sphingomyelin affects alk-SMase expression was examined in a colon cancer animal model. Materials and Methods: Imprinting control region (ICR) mice were injected with 1,2-dimethylhydrazine (DMH) and then fed a diet with or without SM (0.5 g/kg in diet) for 22 weeks. The colonic tumorigenesis and alk-SMase activity were determined and alk-SMase expression was examined by Western blot and PCR. Results: Dietary SM... (More)
- Background: Sphingomyelin (SM) hydrolysis generates biologically active products regulating cell growth, differentiation and apoptosis. Dietary SM has been found to inhibit colonic tumorigenesis. Alkaline sphingomyelinase (alk-SMase) is the key enzyme responsible for sphingomyelin digestion in the gut. Whether or not dietary sphingomyelin affects alk-SMase expression was examined in a colon cancer animal model. Materials and Methods: Imprinting control region (ICR) mice were injected with 1,2-dimethylhydrazine (DMH) and then fed a diet with or without SM (0.5 g/kg in diet) for 22 weeks. The colonic tumorigenesis and alk-SMase activity were determined and alk-SMase expression was examined by Western blot and PCR. Results: Dietary SM inhibited the tumorigenesis and increased the alk-SMase activity in the colon by 65%. The increased activity was associated with increased enzyme protein and mRNA expression. No changes of acid and neutral sphingomyelinase activities were found. Conclusion: Long-term supplementation with dietary sphingomyelin up-regulates colonic alk-SMase expression, which may contribute to the inhibitory effects of sphingomyelin against colonic carcinogenesis. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1376273
- author
- Zhang, Ping ; Li, Baixiang ; Gao, Shuying and Duan, Rui-Dong LU
- organization
- publishing date
- 2008
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Sphingomyelin, alkaline sphingomyelinase, colon cancer, mouse
- in
- Anticancer research
- volume
- 28
- issue
- 6A
- pages
- 3631 - 3635
- publisher
- International Institute of Cancer Research
- external identifiers
-
- wos:000262049100010
- scopus:58149165342
- ISSN
- 1791-7530
- language
- English
- LU publication?
- yes
- id
- 72c2c329-1ee8-4983-961d-4a4283fabb58 (old id 1376273)
- date added to LUP
- 2016-04-01 11:46:37
- date last changed
- 2024-01-07 19:59:25
@article{72c2c329-1ee8-4983-961d-4a4283fabb58,
abstract = {{Background: Sphingomyelin (SM) hydrolysis generates biologically active products regulating cell growth, differentiation and apoptosis. Dietary SM has been found to inhibit colonic tumorigenesis. Alkaline sphingomyelinase (alk-SMase) is the key enzyme responsible for sphingomyelin digestion in the gut. Whether or not dietary sphingomyelin affects alk-SMase expression was examined in a colon cancer animal model. Materials and Methods: Imprinting control region (ICR) mice were injected with 1,2-dimethylhydrazine (DMH) and then fed a diet with or without SM (0.5 g/kg in diet) for 22 weeks. The colonic tumorigenesis and alk-SMase activity were determined and alk-SMase expression was examined by Western blot and PCR. Results: Dietary SM inhibited the tumorigenesis and increased the alk-SMase activity in the colon by 65%. The increased activity was associated with increased enzyme protein and mRNA expression. No changes of acid and neutral sphingomyelinase activities were found. Conclusion: Long-term supplementation with dietary sphingomyelin up-regulates colonic alk-SMase expression, which may contribute to the inhibitory effects of sphingomyelin against colonic carcinogenesis.}},
author = {{Zhang, Ping and Li, Baixiang and Gao, Shuying and Duan, Rui-Dong}},
issn = {{1791-7530}},
keywords = {{Sphingomyelin; alkaline sphingomyelinase; colon cancer; mouse}},
language = {{eng}},
number = {{6A}},
pages = {{3631--3635}},
publisher = {{International Institute of Cancer Research}},
series = {{Anticancer research}},
title = {{Dietary Sphingomyelin Inhibits Colonic Tumorigenesis with an Up-regulation of Alkaline Sphingomyelinase Expression in ICR Mice}},
volume = {{28}},
year = {{2008}},
}