Vitamin D has a definite role in sequential differentiation and orderly progression of keratinocytes from the basal layer of the epidermis. Also, a variety of malignant cells express vitamin D receptors (VDR). Vitamin D has been shown to have an anti-proliferative and pro-differentiating effect on many cell types. This is possibly modulated through stimulation of cell cycle inhibitors p21 and p27, this in turn affects E-cadherin and beta-catenin.
There was an interesting article on the role of vitamin D in colorectal carcinoma in the NEJM in 2006. I am sure that article would be informative.
thanks Vasant Chinnabhandar it was very helpful information i will share it with my colleges specially the article by Jean Watchweski and thank you Nandini you are the first one answering my question
Vitamin D, or more correctly the active 1,25 dihydroxy vitamin D3 inhibits proliferation and enhances differentiation of colonic epithelial cells. These cells express the 1alpha hydroxylase, the enzyme that converts the precursor, 25-D3 into the active form, therefore in colon cancer, serum 25D3 levels are relevant for the preventive effect. Additionally to the mechanisms described by Vasant Chinnabhandar, vitamin D can also inhibit the Wnt pathway and prostaglandine E2 signalling (COX2). It has not only anti-proliferative but also anti-inflammatory effects. There are several very good reviews on the role of vitamin D in colorectal carcinogenesis.
You could do a cross-sectional study, too (similar to a case-control): you take all the people who have colonoscopy during 1 year, and measure their vitamin D. You could assess an eventual gradient between vitamin d concentration and degree of differentiation of the tumour, eventually no cancer / premalignant (adenoma) / malignant (argument for causality). With the weaknesses of such a study (compared to a cohort one) - e.g. which was first, low vitamin d or cancer?