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We began analyzing https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0053287, but it redirected us to https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0053287. The analysis below is for the second page.
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Description:
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 HMLEHRas 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.
Title[redir]:
No title found...
Description:
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 HMLEHRas 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.
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Keywords {🔍}
cells, vdr, cancer, expression, breast, mammospheres, cell, vitamin, article, view, figure, google, scholar, skbr, analysis, fold, mammosphere, tumor, snail, protein, panel, human, aldh, compared, stem, conditions, receptor, significantly, grown, tumors, isolated, significant, plastic, analyzed, combination, treatment, plos, mammary, lines, gene, obtained, levels, sirna, found, high, image, signaling, mcscs, data, growth,
Topics {✒️}
small interfering rna 1371/annotation/5326d117-3f31-4e43-a5c4-9e1fb41719e9 goat anti-mouse alexa-488 androgen receptor complex health cookies plos plos goat anti-rabbit alexa-488 medicine regulating snail/e-cad/emt pathway open-access article distributed contributed reagents/materials/analysis tools nitric-oxide-induced bax integration mouse satellite cells vdr null mouse induces map-kinase phosphatase-1 key cell-surface marker snail/e-cad-mediated pathway original author extracellular signal-regulated kinase initial sep-pak purification sirna sequences–sirna1 5′gcaaccaagacuacaagua3′ pre-dispensed primer sets e-cad protein expression serum-free mammosphere media full-length human vdr cell-specific gene sets enhance anti-proliferative effects emt-specific gene signature ultra-low attachment plates aggressive breast tumors serum-free culture medium enhanced anti-proliferative effects including breast tumors advanced solid tumors anti-proliferative target genes human pcr primers map-kinase phosphatase -1 human mammary epithelial mg cellular protein transmembrane protein 132a driving aggressive tumors e-cad protein charles drew university mediating testosterone action growth factor independence g-protein signaling 2 t-cell factor 4 10–12% sds-page gels facilitate bax integration
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