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Vitamin D may slow pre-cancer growths, find researchers

By Nathan Gray , 28-Nov-2012

Vitamin D may help to battle cancers by blocking cell growth and slowing the progression of pre-malignant to malignant states, say researchers.

The team of Canadian researchers said the newly discovered mechanism provides a molecular basis for the potential cancer preventive effects of vitamin D.

Writing in the Proceedings of the National Academy of Sciences (PNAS), the authors report that the active form of vitamin D acts to block cancer formation by several mechanisms that inhibit both the production and function of a specific protein required for cell division (known as cMYC).

Led by Professor John White, the research team explained that cMYC drives cell division and is active at elevated levels in more than half of all cancers, however, the new findings suggest vitamin D alter this situation.

"We discovered that vitamin D controls both the rate of production and the degradation of cMYC,” said White.

“More importantly, we found that vitamin D strongly stimulates the production of a natural antagonist of cMYC called MXD1, essentially shutting down cMYC function,” he said.

The team said vitamin D acts to suppress the expression of genes regulated by c-MYC and enhanced MXD1 expression and stability, “dramatically altering ratios of DNA-bound c-MYC and MXD1.”

"Our results show that vitamin D puts the brakes on cMYC function, suggesting that it may slow the progression of cells from premalignant to malignant states and keep their proliferation in check,” said White.

We hope that our research will encourage people to maintain adequate vitamin D supplementation and will stimulate the development of large, well-controlled cancer chemoprevention trials to test the effects of adequate supplementation," he added.

Source: PNAS
Published online, open access, doi: 10.1073/pnas.1210037109
“Vitamin D receptor as a master regulator of the c-MYC/MXD1 network”
Authors: Reyhaneh Salehi-Tabar, Loan Nguyen-Yamamoto, Luz E. Tavera-Mendoza, Thomas Quail, et al

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