Micro RNA involved in vitamin d to against cancer

The anticancer effect of vitamin d has been recognized, but it is the treatment of cancer applications is hindered by the side effects caused by its super-physiological concentrations. Therefore, to explore the mechanism of tumor suppression function of vitamin d can promote the improvement of the clinical application. The researchers, devoted themselves to the research of micro RNA and vitamin d anticancer.

Vitamin d is both a vitamin, also a steroid hormone, is divided into two kinds of endogenous and exogenous, endogenous human skin in 7-dehydrocholesterol by ultraviolet radiation of wavelength 290~320mm first converted to vitaminD3 precursor in body temperature effect gradually transformed into vitamin D3 (cholecalciferol bile calciferol). It is in the form of chylomicron in the small intestine to absorb bile salts to promote its absorption. With the combination of ? globulin (DBP) blood transit, first in the liver mitochondria after 25-hydroxylase system role into a 25-(OH) D, followed by transporters to the renal proximal tubule epithelial cells in the mitochondria by the hydroxylase role generate 1,25 (OH) 2D3, which is the most active derivatives of vitamin D metabolism. Vitamin d in addition to the important role of the intestine, bone, kidney, still in the stratum corneum of the skin cells, islet cells, lymphocytes early promyelocytic cells found in the vitamin d receptor found in recent studies, in addition, 1,25 (OH ) 2D3 on lymphocyte proliferation and differentiation of the monocyte-macrophage cells and thymocytes have more far-reaching impact factor as an immunomodulator, 1,25 (OH) 2D3 also attracted peoples attention.

The researchers first use chip technology, vitamin d response microRNA expression in LNCaP cell lines screened, (the miRNA chips Services provided by LC biological), discovered a tumor suppressor gene of miR-98 in LNCaP cells by 1?, 25 two hydroxy vitamin D3 (1,25-VD) induced expression. The mechanism analysis results show 1,25-VD-induced miR-98 Jibei direct mechanism for enhanced miR-98 to start the promoter region of VDR binding response element, indirect mechanism down LIN-28 expression mediated by. The researchers found that the knockout miR-98 led to anti-growth effect of 1,25-VD decreases, whereas overexpression of miR-98-induced G2/M arrest and inhibition of the growth of LNCaP cells. miR-98 down CCNJ (control of cell the mitotic protein) expression levels through its targeted CCNJ 3-untranslated region. Interestingly, the miR-98 level in the blood of mice of the 1,25-VD treatment will rise, indicating that the miR-98 is predicted 1,25-VD response potential biomarkers.

The study of micro RNA involved in vitamin d to against cancer found that 1,25-VD-induced growth inhibition of sex of miR-98, provides a potential therapeutic target for prostate cancer, but also provide a potential biomarker for the anticancer effects of 1,25-VD.
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