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Lab Study Suggests Low Vitamin D Spurs Oral Cell Growth

head musculatureCurrently, there is no clear link between vitamin D and lower risk of cancer, yet numerous lab studies suggest the hormone may play a role in lowering risk of certain types of cancers. Now, a study in mice focusing on oral cancers has found that consuming a diet low in vitamin D results in cell proliferation, a hallmark of cancer development.

The study was published last week in the International Journal of Oncology and it was funded by AICR.

For the study, researchers first determined the role of vitamin D signaling in oral cells. The study used a type of cell called keratinocytes, which are the major type of cell in the upper layer of our skin. On skin keratinocytes, research has already found that vitamin D inhibits cell proliferation and differentiation. Far less is known about the role of vitamin D on oral keratinocytes.

In oral keratinocytes cells without a vitamin D receptor, which vitamin D binds to, cells proliferated more rapidly than the cells with a vitamin D receptor.

Researchers then conducted an animal study. For four months, one group of mice ate a diet low in vitamin D while the other group ate a diet with sufficient vitamin D. When the study was over the animals deficient in the active form of vitamin D – 25OHD – had a modest but significant increase in cell proliferation on their tongues. Vitamin D deficiency alone did not stimulate oral cancer, but as the authors note, it raises the possibility that lower levels of 25OHD may contribute in part to oral cancers. Possibly consuming a vitamin D deficient diet for longer or a more severe vitamin D-deficiency diet may promote carcinogenesis, the study notes.


Source: Feng-Ning F. Yuan, Jayasanker Valiyaparambil, Michael C. Woods, Huy Tran, Rima Pant, John S. Adams, Sanjay M. Mallya. "Vitamin D signaling regulates oral keratinocyte proliferation in vitro and in vivo." International Journal of Oncology. Volume 44 Issue 5, Published online first March 12, 2014.

Published on April 2, 2014

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