Format

Send to

Choose Destination
Nutr Cancer. 2016 Oct;68(7):1202-9. doi: 10.1080/01635581.2016.1213868. Epub 2016 Aug 23.

1α,25-Dihydroxyvitamin D Inhibits the Metastatic Capability of MCF10CA1a and MDA-MB-231 Cells in an In Vitro Model of Breast to Bone Metastasis.

Author information

1
a Department of Nutrition Science, Interdepartmental Nutrition Program , Purdue University , West Lafayette , Indiana , USA.
2
b Interdisciplinary Life Science-PULSe , Purdue University , West Lafayette , Indiana , USA.
3
c Department of Biological Sciences , Purdue University , West Lafayette , Indiana , USA.
4
d Ixchel Scientific , San Jose , California , USA.

Abstract

Breast cancer metastasis to the bone continues to be a major health problem, with approximately 80% of advanced breast cancer patients expected to develop bone metastasis. Although the problem of bone metastasis persists, current treatment options for metastatic cancer patients are limited. In this study, we investigated the preventive role of the active vitamin D metabolite, 1α,25-dihydroxyvitamin D (1,25(OH)2D), against the metastatic potential of breast cancer cells using a novel three-dimensional model (rMET) recapitulating multiple steps of the bone metastatic process. Treatment of MCF10CA1a and MDA-MB-231 cells inhibited metastasis in the rMET model by 70% (±5.7%) and 21% (±6%), respectively. In addition, 1,25(OH)2D treatment decreased invasiveness (20 ± 11% of vehicle) and decreased the capability of MCF10CA1a cells to survive in the reconstructed bone environment after successful invasion through the basement membrane (69 ± 5% of vehicle). An essential step in metastasis is epithelial-mesenchymal transition (EMT). Treatment of MCF10CA1a cells with 1,25(OH)2D increased gene (2.04 ± 0.28-fold increase) and protein (1.87 ± 0.20-fold increase) expression of E-cadherin. Additionally, 1,25(OH)2D treatment decreased N-cadherin gene expression (42 ± 8% decrease), a marker for EMT. Collectively, the present study suggests that 1,25(OH)2D inhibits breast cancer cell metastatic capability as well as inhibits EMT, an essential step in the metastatic process.

PMID:
27552186
PMCID:
PMC5047026
DOI:
10.1080/01635581.2016.1213868
[Indexed for MEDLINE]
Free PMC Article

Conflict of interest statement

The authors declare that they have no conflict of interest.

Publication types, MeSH terms, Substances, Grant support

Publication types

MeSH terms

Substances

Grant support

Supplemental Content

Full text links

Icon for PubMed Central
Loading ...
Support Center