Functions of 1α,25-dihydroxyvitamin D3 in mammary gland: from normal development to breast cancer

  title={Functions of 1$\alpha$,25-dihydroxyvitamin D3 in mammary gland: from normal development to breast cancer},
  author={Carmen J. Narvaez and Glendon M. Zinser and JoEllen Welsh},

A Role for Interleukin-1 Alpha in the 1,25 Dihydroxyvitamin D3 Response in Mammary Epithelial Cells

Findings support the chemopreventative potential of vitamin D3 in the mammary gland and present a role for IL1α in regulation of mammary cell proliferation by 1,25(OH)2D3.

Impact of the Vitamin D3 receptor on growth-regulatory pathways in mammary gland and breast cancer

Mechanisms implicated in the growth regulatory effects of vitamin D in breast cancer.

It is now well established that, in addition to its central role in the maintenance of extracellular calcium levels and bone mineralization, 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)), the active

Nutritional Genomics in Cancer Processes Vitamin D-3 Receptor as a Target for Breast Cancer Prevention 1 , 2

Findings from cellular, molecular and population studies suggest that the VDR is a nutritionally modulated growth-regulatory gene that may represent amolecular target for chemoprevention of breast cancer.

Vitamin D and cancer: an update of in vitro and in vivo data.

Empirical and experimental in vitro and in vivo data support a cancer preventive role of 1,25(OH)2D3, and multiple analogs with reduced calcemic properties, which are thus less toxic, are under investigation.

Antiproliferative action of menadione and 1,25(OH)2D3 on breast cancer cells

Vitamin D-3 receptor as a target for breast cancer prevention.

Findings from cellular, molecular and population studies suggest that the VDR is a nutritionally modulated growth-regulatory gene that may represent a molecular target for chemoprevention of breast cancer.

Vitamin D regulates the phenotype of human breast cancer cells.

Findings show that 1,25(OH)(2)D(3) profoundly affects the phenotype of breast cancer cells, and suggest that it reverts the myoepithelial features associated with more aggressive forms and poor prognosis in human breast cancer.



Characterization of a vitamin D3-resistant MCF-7 cell line.

MCF-7D3Res cells offer a unique model system for identification of the mechanisms by which vitamin D3 regulates the cell death pathway in breast cancer cells, and are suggested to have a functional VDR that is uncoupled from a functional apoptotic pathway.

Induction of apoptosis in breast cancer cells in response to vitamin D and antiestrogens.

  • J. Welsh
  • Biology, Chemistry
    Biochemistry and cell biology = Biochimie et biologie cellulaire
  • 1994
It is shown that apoptosis can be induced in MCF-7 cells either by activation of vitamin-D-mediated signalling or disruption of estrogen-dependent signalling, and combined treatment with 1,25(OH)2D3 and TAM enhances the degree of apoptosis assessed using morphological markers.

Role of apoptosis in the growth inhibitory effects of vitamin D in MCF-7 cells.

Studies from a number of laboratories have clearly demonstrated that 1,25(OH)2D3 inhibits growth of breast cancer cells in vitro, and causes regression of tumors growing in vivo, however, the underlying mechanism of the effect of vitamin D has yet to be clarified.

Differential effects of 1,25-dihydroxyvitamin D3 and tetradecanoylphorbol acetate on cell cycle and apoptosis of MCF-7 cells and a vitamin D3-resistant variant.

It is concluded that cell cycle arrest is not sufficient to trigger cell death of MCF-7 cells, and that 1,25-(OH)2D3 generates distinct signals which lead to induction of apoptosis in breast cancer cells.

Effects of 1,25 dihydroxyvitamin D3 and its analogues on induction of apoptosis in breast cancer cells

1,25 Dihydroxyvitamin D3: Coordinate Regulator of Active Cell Death and Proliferation in MCF-7 Breast Cancer Cells

This work has shown that in vitro, apoptotic cells and bodies can be recovered in the media, whereas in vivo, these are removed by phagocytic macrophages, and in some, but not all, forms of ACD, cleavage of DNA into large fragments and further degradation into 200-bp fragments, characteristic of a nucleosome ladder, can be demonstrated.

1,25-Dihydroxyvitamin D3 enhances the susceptibility of breast cancer cells to doxorubicin-induced oxidative damage.

Results indicate that ROS are involved in the interaction between 1,25(OH)2D3 and doxorubicin, and suggest increased efficacy of 1, 25(OH), the hormonal form of vitamin D, or its analogues in combination with other ROS-generating anticancer therapeutic modalities.

Apoptosis induced by vitamin D compounds in breast cancer cells is inhibited by Bcl-2 but does not involve known caspases or p53.

Data indicate that vitamin D compounds induce apoptosis via a novel caspase- and p53-independent pathway that can be inhibited by Bcl-2, which may prove useful in the treatment of tumors that are resistant to therapeutic agents that are dependent on the activation of p53 and/or caspases.