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Br J Nutr. 2016 May;115(9):1643-60. doi: 10.1017/S0007114516000696.

Vitamin D and colorectal cancer: molecular, epidemiological and clinical evidence.

Author information

  • 11Department of Medical Oncology,Dana-Farber Cancer Institute and Harvard Medical School, 450 Brookline Avenue,Boston,MA 02215,USA.
  • 23Department of Nutrition,Harvard T. H. Chan School of Public Health, 677 Huntington Avenue,Boston,MA 02115,USA.

Abstract

In many cells throughout the body, vitamin D is converted into its active form calcitriol and binds to the vitamin D receptor (VDR), which functions as a transcription factor to regulate various biological processes including cellular differentiation and immune response. Vitamin D-metabolising enzymes (including CYP24A1 and CYP27B1) and VDR play major roles in exerting and regulating the effects of vitamin D. Preclinical and epidemiological studies have provided evidence for anti-cancer effects of vitamin D (particularly against colorectal cancer), although clinical trials have yet to prove its benefit. In addition, molecular pathological epidemiology research can provide insights into the interaction of vitamin D with tumour molecular and immunity status. Other future research directions include genome-wide research on VDR transcriptional targets, gene-environment interaction analyses and clinical trials on vitamin D efficacy in colorectal cancer patients. In this study, we review the literature on vitamin D and colorectal cancer from both mechanistic and population studies and discuss the links and controversies within and between the two parts of evidence.

KEYWORDS:

25(OH)D 25-Hydroxyvitamin D; 25-Hydroxyvitamin D; CDK cyclin-dependent kinase; MPE molecular pathological epidemiology; P450 hydroxylases; VDR vitamin D receptor; Vitamin D supplementation; miR microRNA

PMID:
27245104
PMCID:
PMC4890569
[Available on 2017-05-01]
DOI:
10.1017/S0007114516000696
[PubMed - in process]
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