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Down-regulation of vitamin D receptor in mammospheres: implications for vitamin D resistance in breast cancer and potential for combination therapy.
- Source :
-
PloS one [PLoS One] 2013; Vol. 8 (1), pp. e53287. Date of Electronic Publication: 2013 Jan 14. - Publication Year :
- 2013
-
Abstract
- Vitamin D signaling in mammary cancer stem cells (MCSCs), which are implicated in the initiation and progression of breast cancer, is poorly understood. In this study, we examined vitamin D signaling in mammospheres which are enriched in MCSCs from established breast cancer cell lines. Breast cancer cells positive for aldehyde dehydrogenase (ALDH(+)) had increased ability to form mammospheres compared to ALDH(-) cells. These mammospheres expressed MCSC-specific markers and generated transplantable xenografts in nude mice. Vitamin D receptor (VDR) was significantly down-regulated in mammospheres, as well as in ALDH(+) breast cancer cells. TN aggressive human breast tumors as well as transplantable xenografts obtained from SKBR3 expressed significantly lower levels of VDR but higher levels of CD44 expression. Snail was up-regulated in mammospheres isolated from breast cancer cells. Inhibition of VDR expression by siRNA led to a significant change in key EMT-specific transcription factors and increased the ability of these cells to form mammospheres. On the other hand, over-expression of VDR led to a down-regulation of Snail but increased expression of E-cad and significantly compromised the ability of cells to form mammospheres. Mammospheres were relatively insensitive to treatment with 1,25-dihydroxyvitamin D (1,25D), the active form of vitamin D, compared to more differentiated cancer cells grown in presence of serum. Treatment of H-Ras transformed HMLE(HRas) cells with DETA NONOate, a nitric oxide (NO)-donor led to induction of MAP-kinase phosphatase -1 (MKP-1) and dephosphorylation of ERK1/2 in the mammospheres. Combined treatment of these cells with 1,25D and a low-concentration of DETA NONOate led to a significant decrease in the overall size of mammospheres and reduced tumor volume in nude mice. Our findings therefore, suggest that combination therapy using 1,25D with drugs specifically targeting key survival pathways in MCSCs warrant testing in prospective clinical trial for treatment of aggressive breast cancer.
- Subjects :
- Animals
Antineoplastic Combined Chemotherapy Protocols pharmacology
Antineoplastic Combined Chemotherapy Protocols therapeutic use
Breast Neoplasms enzymology
Breast Neoplasms genetics
Breast Neoplasms pathology
Cell Line, Tumor
Cell Separation
Down-Regulation drug effects
Drug Resistance, Neoplasm genetics
Epithelial-Mesenchymal Transition drug effects
Epithelial-Mesenchymal Transition genetics
Female
Gene Expression Profiling
Gene Expression Regulation, Neoplastic drug effects
Humans
Hyaluronan Receptors metabolism
Intercellular Signaling Peptides and Proteins pharmacology
Mammary Glands, Human drug effects
Mice
Mice, Nude
Neoplastic Stem Cells drug effects
Neoplastic Stem Cells metabolism
Neoplastic Stem Cells pathology
Nitric Oxide pharmacology
Retinoid X Receptors metabolism
Snail Family Transcription Factors
Spheroids, Cellular drug effects
Spheroids, Cellular metabolism
Transcription Factors metabolism
Up-Regulation drug effects
Up-Regulation genetics
Vitamin D pharmacology
Vitamin D therapeutic use
Xenograft Model Antitumor Assays
Breast Neoplasms drug therapy
Down-Regulation genetics
Drug Resistance, Neoplasm drug effects
Mammary Glands, Human pathology
Receptors, Calcitriol genetics
Spheroids, Cellular pathology
Vitamin D analogs & derivatives
Subjects
Details
- Language :
- English
- ISSN :
- 1932-6203
- Volume :
- 8
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- PloS one
- Publication Type :
- Academic Journal
- Accession number :
- 23341935
- Full Text :
- https://doi.org/10.1371/journal.pone.0053287