期刊
HORMONE MOLECULAR BIOLOGY AND CLINICAL INVESTIGATION
卷 20, 期 2, 页码 43-49出版社
WALTER DE GRUYTER GMBH
DOI: 10.1515/hmbci-2014-0035
关键词
apoptosis; calpains; cancer; caspases; intracellular Ca2+; obesity; vitamin D
资金
- National Institutes of Health [1R15CA067317-01A1, 7R15CA067317-02]
- US Department of Agriculture [SD00179-H, SD00294-H, SD00325-H, SD00H167-061HG, 2009-35200-05008]
- NIFA [2009-35200-05008, 582614] Funding Source: Federal RePORTER
Low vitamin D status has been associated with increased risk of several cancers and obesity; concurrently, obesity and cancer have been linked to impaired vitamin D status. In both cancer and obesity, selective elimination of cancer cells and adipocytes can result in decreasing tumor size and a long-term reduction in adipose tissue mass. These effects can be achieved through induction of apoptotic cell death. The vitamin D-derived hormone 1,25-dihydroxyvitamin D-3 (1,25(OH)(2)D-3) triggers apoptosis in epithelial cancer cells and mature adipocytes via induction of apoptotic Ca2+ signal - a sustained, prolonged increase in concentration of intracellular Ca2+. This Ca2+ signal functions as an apoptotic initiator that directly recruits apoptotic effectors, Ca2+-dependent proteases, in cancer cells and adipocytes. The 1,25(OH)(2)D-3 - cellular Ca2+ - apoptosis link in cancer and obesity supports the rationale to include vitamin D compounds modulating intracellular Ca2+ and Ca2+-dependent apoptotic proteases as promising targets for discovery of new therapeutic and preventive agents for cancer and obesity. The concept of maintaining an increased vitamin D status for protecting against cancer and decreasing adiposity also warrants further evaluation.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据