Source:http://linkedlifedata.com/resource/pubmed/id/16177194
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
10
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pubmed:dateCreated |
2005-9-22
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pubmed:abstractText |
Vitamin D deficiency has been associated with increased risk of colon cancer in epidemiologic and prospective clinical studies. In vitro and in vivo studies demonstrated that 1,25-dihydroxycholecalciferol [1,25(OH)2D3] and its analogs inhibit colon cancer cell proliferation. Few studies have evaluated the effect of vitamin D deficiency on the development and growth of colon cancer. To assess the antiproliferative effects of 25-hydroxyvitamin D [25(OH)D] and 1,25(OH)2D3 in vitro, we cultured MC-26 (a colon cancer cell line) in the presence of 25(OH)D3 and 1,25(OH)2D3 and performed [3H]thymidine incorporation. The proliferation of MC-26 was significantly inhibited by both 25(OH)D3 and 1,25(OH)2D3. To determine the effect of vitamin D deficiency on colon cancer proliferation, Balb/c mice were rendered vitamin D deficient by feeding them a vitamin D-deficient diet for 3 mo. A group of vitamin D-sufficient mice was given the same diet with supplemental vitamin D. The mice were injected with MC-26 colon cancer cells and the tumors were measured daily for 20 d. Vitamin D-sufficient mice had 40% smaller tumors than vitamin D-deficient mice. The tumors were evaluated for mRNA expression of the vitamin D receptor (VDR) and 25-hydroxvitamin D-1alpha-hydroxylase (1alpha-OHase) by quantitative RT-PCR. The expression of the mRNA for the VDR and the 1alpha-OHase was 37- and 6-fold higher, respectively, in the vitamin D-sufficient mice compared with the vitamin D-deficient mice. We conclude that vitamin D deficiency enhances the growth of colon cancer in mice. The tumor expression of VDR and 1alpha-OHase indicates possible autocrine/paracrine cell growth regulation by vitamin D.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0022-3166
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
135
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2350-4
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:16177194-25-Hydroxyvitamin D3 1-alpha-Hydroxylase,
pubmed-meshheading:16177194-Animals,
pubmed-meshheading:16177194-Calcitriol,
pubmed-meshheading:16177194-Cell Division,
pubmed-meshheading:16177194-Cell Line, Tumor,
pubmed-meshheading:16177194-Colonic Neoplasms,
pubmed-meshheading:16177194-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:16177194-Mice,
pubmed-meshheading:16177194-Mice, Inbred BALB C,
pubmed-meshheading:16177194-Neoplasm Transplantation,
pubmed-meshheading:16177194-Receptors, Calcitriol,
pubmed-meshheading:16177194-Transplantation, Heterologous,
pubmed-meshheading:16177194-Vitamin D Deficiency,
pubmed-meshheading:16177194-Vitamins
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pubmed:year |
2005
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pubmed:articleTitle |
Vitamin D deficiency enhances the growth of MC-26 colon cancer xenografts in Balb/c mice.
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pubmed:affiliation |
Division of Endocrinology, Diabetes and Lipids, Department of Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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