The Journal of Steroid Biochemistry and Molecular Biology, online 4 July 2018, https://doi.org/10.1016/j.jsbmb.2018.07.002
Gemma Ferrer-Mayorga María Jesús Larribaa Piero Crespo Alberto Muñoza
- Colorectal cancer is the neoplasia that is most closely linked to vitamin D deficiency in epidemiological studies.
- Calcitriol inhibits the proliferation, migration, invasiveness and angiogenesis of colon carcinoma cells, and promotes their differentiation and sensitizes them to apoptosis.
- Calcitriol reduces the protumoral effects of colon cancer-associated fibroblasts.
- Calcitriol also regulates the biology of intestinal immune cells and affects the intestinal microbiota.
- Cancer - Colon category listing has
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- Advanced Colon Cancer risk is doubled or halved with 1000 IU of Vitamin D, depends on Vitamin D Receptors – RCT May 2017
- Colon Cancer survival 3.1 X less likely if poor Vitamin D Receptor – Aug 2017
The Meta-analysis of many studies of COLON Cancer and Vitamin D are listed here:
- Colorectal cancer is associated with Vitamin D (17 meta-analyses so far) – July 2018
- Colorectal cancer 60 percent less likely: high vs low Vitamin D level – meta-analysis Dec 2016
- Colorectal Cancer recurrence not prevented by 1,000 IU of vitamin D – meta-analysis Dec 2016
- Risk of Cancer increased if poor Vitamin D Receptor – meta-analysis of 73 studies Jan 2016
- Colon cancer 30 percent more likely if low vitamin D – 12th meta-analysis Aug 2015
- Colon cancer risk reduced by many vitamins – 13 percent reduction by Vitamin D – meta-analysis Jan 2015
- Cancer (colon, breast, lymph) survival about 2X better with high level vitamin D – meta-analysis July 2014
- Cancer survival 4 percent more likely with just a little more vitamin D (4 ng) - meta-analysis July 2014
- Colorectal and Breast Cancer – Vitamin D is associated with fewer deaths – meta-analysis Feb 2014
- 10 percent of colon cancer linked to Vitamin D Receptor – meta-analysis April 2012
- Meta-graphs of vitamin D and Cancer – Dec 2011
- Colon cancer probability increases with decreased vitamin D – Meta-analysis July 2011
- Non-cancer colon growths 7 percent less likely with each 10 ng increase in vitamin D – Oct 2011
- Colorectal cancer 26 percent less likely for every 10 ng of vitamin D – meta-analysis Aug 2011
- Colon polyps reduced 15 percent by increasing vitamin D by 20 ng – meta-analysis June 2011
- Meta-analysis of 3 cancers - 10 ng more vitamin D decrease colorectal by 15 percent– May 2010
- Meta-analysis found vitamin D association with colon but not prostate nor breast cancer May 2010
Accepted manuscript PDF is available free at Sci-Hub 10.1016/j.jsbmb.2018.07.002
Colorectal cancer (CRC) is the neoplasia that is most frequently associated with vitamin D deficiency in epidemiological and observational studies in terms of incidence and mortality. Many mechanistic studies show that the active vitamin D metabolite (1α,25-dihydroxyvitamin D3 or calcitriol) inhibits proliferation and promotes epithelial differentiation of human colon carcinoma cell lines that express vitamin D receptor (VDR) via the regulation of a high number of genes. A key action underlining this effect is the multilevel inhibition of the Wnt/β-catenin signaling pathway, whose abnormal activation in colon epithelial cells initiates and promotes CRC. Recently, our group has shown that calcitriol modulates gene expression and inhibits protumoral properties of patient-derived colon cancer-associated fibroblasts (CAFs). Accordingly, high VDR expression in tumor stromal fibroblasts is associated with longer survival of CRC patients. Moreover, many types of immune cells express VDR and are regulated by calcitriol, which probably contributes to its action against CRC. Given the role attributed to the intestinal microbiota in CRC and the finding that it is altered by vitamin D deficiency, an indirect antitumoral effect of calcitriol is also plausible at this level. In summary, calcitriol has an array of potential protective effects against CRC by acting on carcinoma cells, CAFs, immune cells and probably also the gut microbiota.