The transcription factor SNAIL represses vitamin D receptor expression and responsiveness in human colon cancer

2004 ◽  
Vol 10 (9) ◽  
pp. 917-919 ◽  
Author(s):  
Héctor G Pálmer ◽  
María Jesús Larriba ◽  
José Miguel García ◽  
Paloma Ordóñez-Morán ◽  
Cristina Peña ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Vitamin D ◽  
Transcription Factor ◽  
Vitamin D Receptor ◽  
Human Colon ◽  
Receptor Expression ◽  
Human Colon Cancer

scholarly journals p38 MAPK Activation Selectively Induces Cell Death in K-ras-mutated Human Colon Cancer Cells through Regulation of Vitamin D Receptor

2004 ◽  
Vol 279 (21) ◽  
pp. 22138-22144 ◽  
Author(s):  
Xiaomei Qi ◽  
Jun Tang ◽  
Rocky Pramanik ◽  
Richard M. Schultz ◽  
Senji Shirasawa ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Vitamin D ◽  
Cell Death ◽  
Cancer Cells ◽  
Vitamin D Receptor ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Mapk Activation ◽  
Human Colon Cancer Cells

scholarly journals Vitamin D receptor protects against dysbiosis and tumorigenesis via the JAK/STAT pathway in intestine

2020 ◽  
Author(s):  
Yong-Guo Zhang ◽  
Rong Lu ◽  
Shaoping Wu ◽  
Ishita Chatterjee ◽  
David Zhou ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Vitamin D ◽  
Vitamin D Receptor ◽  
Human Colon ◽  
Fecal Microbiota ◽  
Proximal Colon ◽  
Conditional Knockout ◽  
Human Colon Cancer ◽  
Gene Variation ◽  
Stat Pathway

AbstractBackgroundVitamin D exerts regulatory roles via vitamin D receptor (VDR) in mucosal immunity, host defense, and inflammation involving host factors and microbiome. Human Vdr gene variation shapes the microbiome and VDR deletion leads to dysbiosis. Low VDR expression and diminished vitamin D/VDR signaling are observed in colon cancer. Nevertheless, how intestinal epithelial VDR is involved in tumorigenesis through gut microbiota remains unknown. We hypothesized that intestinal VDR protects mice against dysbiosis via modulating the JAK/STAT pathway in tumorigenesis. To test our hypothesis, we used an azoxymethane/Dextran Sulfate Sodium-induced cancer model in intestinal VDR conditional knockout (VDRΔIEC) mice, cell cultures, stem-cell derived colonoids, and human colon cancer samples.ResultsVDRΔIEC mice have higher numbers of tumors with location shifted from distal to proximal colon. Fecal microbiota analysis showed that VDR deletion leads to bacterial profile shift from normal to susceptible carcinogenesis. We found enhanced bacterial staining in mouse and human tumors. Microbial metabolites from VDRΔIEC mice showed elevated secondary bile acids, consistent with the observations in human CRC. We further identified that VDR protein bound to the Jak2 promoter, suggesting that VDR transcriptionally regulated Jak2. The JAK/STAT pathway is critical in intestinal and microbial homeostasis. Fecal samples from VDRΔIEC mice activate the STAT3 activation in human and mouse organoids. Lack of VDR led to hyperfunction of Jak2 in respond to intestinal dysbiosis. A JAK/STAT inhibitor abolished the microbiome-induced activation of STAT3.ConclusionWe provide insights into the mechanism of VDR dysfunction leading to dysbiosis and tumorigenesis. It indicates a new target — microbiome and VDR for prevention of cancer.

25-Hydroxy-Vitamin D Metabolism in Human Colon Cancer Cells during Tumor Progression

2001 ◽  
Vol 285 (4) ◽  
pp. 1012-1017 ◽  
Author(s):  
Petra Bareis ◽  
Giovanna Bises ◽  
Martin G. Bischof ◽  
Heide S. Cross ◽  
Meinrad Peterlik
Keyword(s):  
Colon Cancer ◽  
Vitamin D ◽  
Tumor Progression ◽  
Cancer Cells ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Vitamin D Metabolism ◽  
25 Hydroxy Vitamin D ◽  
Human Colon Cancer Cells
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