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Comment
. 2009 Mar;2(3):197-9.
doi: 10.1158/1940-6207.CAPR-09-0019. Epub 2009 Mar 3.

Vitamin D, calcium, and colorectal neoplasia: new insights on mechanisms of action

Elizabeth T Jacobs  1 , Peter W Jurutka, María Elena Martínez, David S Alberts
Affiliations
Comment

Vitamin D, calcium, and colorectal neoplasia: new insights on mechanisms of action

Elizabeth T Jacobs et al. Cancer Prev Res (Phila). 2009 Mar.
No abstract available

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Figures

Fig. 1
Fig. 1
Interactions between vitamin D and calcium in colorectal carcinogenesis. A, regarding the intricate biological relationship between calcium (Ca2+) and vitamin D homeostasis, higher concentrations of Ca2+ inhibit the secretion of parathyroid hormone (PTH); the lack of PTH downregulates CYP27B1 activity, leading ultimately to lower circulating concentrations of 1,25(OH)2D3, the hormonal form of vitamin D. In turn, this effect would reduce the 1,25(OH)2D3-stimulated apoptosis that is illustrated in panel B [colon crypt modified from Humphries and Wright(27)]. B, calcium has a critical role in regulating cell, or colonocyte, turnover in colon crypts. The presence of calcium may have pro-differentiative and/or pro-apoptotic effects, depending on the state of the cell as well as its location in the crypt. As cells move toward the lumen in normal crypts, the presence of Ca2+ stimulates terminal differentiation via binding to and activation of calcium-sensing receptors (CaSRs). As cells reach the mucosal surface, Ca2+ can induce apoptosis. However, in adenomatous crypts, Ca2+ may actually stimulate proliferation and the production of apoptosis-resistant cells.
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