Oops, you're using an old version of your browser so some of the features on this page may not be displaying properly.

MINIMAL Requirements: Google Chrome 24+Mozilla Firefox 20+Internet Explorer 11Opera 15–18Apple Safari 7SeaMonkey 2.15-2.23

Poster presentation 1

1284 - Vitamin D3 (cholecalciferol) acts as a negative regulator of breast cancer cell invasiveness in the absence of activation of classical VDR signalling


19 Dec 2015


Poster presentation 1


MD Musharraf Hossain


Annals of Oncology (2015) 26 (suppl_9): 1-7. 10.1093/annonc/mdv517


M.M. Hossain1, R. Afroz2, C.R. Dunstan2

Author affiliations

  • 1 Biomedical Engineering, The University of Sydney, 2006 - Sydney/AU
  • 2 Biomedical Engineering, University of Sydney, 2006 - Sydney/AU


Abstract 1284


Vitamin D deficiency is a risk factor for breast cancer and is associated with worse breast cancer outcomes. However the mechanisms by which vitamin D3, also known as cholecalciferol and its bioactive metabolite 1α,25 dihydroxyvitamin D3 (1,25(OH)2D3) act to influence breast cancer is not fully resolved. Cholecalciferol is thought to be a biologically inert precursor for bioactive 1,25(OH)2D3and can be converted into the active form by 25-hydroxylase and 1α-hydroxylase enzymes in the liver and kidney respectively. It has been shown that 1,25(OH)2D3 inhibits cancer cell proliferation and migration but a role for cholecalciferol itself in breast cancer has not been defined.


We investigated the in vitro effects of cholecalciferol and 1,25(OH)2D3 on the growth (MTT assay), and invasiveness (Matrigel droplet escape) for the human breast cancer cell lines MDA-MB-231 and MCF-7.


As expected, we showed that 1,25(OH)2D3 inhibits both cancer cell growth and invasiveness . Interestingly for both cell lines, we also found that cholecalciferol reduces cancer cell invasiveness at a concentration of 10−7 M while having no effects on cell growth. CYP24, encoding the enzyme that degrades 1,25(OH)2D3, is an early response gene for vitamin D receptor (VDR) activation. 1,25(OH)2D3 at 10−7M profoundly increased CYP24 expression by 37 fold on day 1 (p < 0.001) and 9 fold on day 3 (p < 0.001)in MDA-MB-231 cells and 243 fold on day 3(p < 0.001) in MCF-7 cells indicating activation of the VDR in MDA-MB-231 and MCF-7 cells. In contrast, CYP24 levels were not changed by cholecalciferol treatment.


Cholecalciferol had no effect on CYP24 gene expression indicating its actions were not initiated via classical activation of the VDR. These results suggest that cholecalciferol has a biological effect on the migration of breast cancer cells that may be independent of the VDR.

Clinical trial identification


All authors have declared no conflicts of interest.

This site uses cookies. Some of these cookies are essential, while others help us improve your experience by providing insights into how the site is being used.

For more detailed information on the cookies we use, please check our Privacy Policy.

Customise settings