Department of Internal Medicine, Charles Drew University of Medicine and Science, Los Angeles, CA, USA.
PLoS One. 2013;8(1):e53287. doi: 10.1371/journal.pone.0053287. Epub 2013 Jan 14.
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.
维生素 D 在乳腺肿瘤干细胞(MCSCs)中的信号转导作用,其与乳腺癌的发生和发展有关,但目前了解甚少。在这项研究中,我们研究了在乳腺球体中的维生素 D 信号转导,这些球体富含来自已建立的乳腺癌细胞系中的 MCSCs。醛脱氢酶(ALDH)阳性的乳腺癌细胞比 ALDH 阴性细胞具有更高的形成乳腺球体的能力。这些乳腺球体表达了 MCSC 特异性标志物,并在裸鼠中生成了可移植的异种移植物。维生素 D 受体(VDR)在乳腺球体以及 ALDH 阳性的乳腺癌细胞中均显著下调。TN 侵袭性人乳腺肿瘤以及从 SKBR3 获得的可移植异种移植物表达的 VDR 水平明显较低,但 CD44 的表达水平较高。Snail 在从乳腺癌细胞中分离的乳腺球体中上调。用 siRNA 抑制 VDR 表达导致 EMT 特异性转录因子的关键变化,并增加了这些细胞形成乳腺球体的能力。另一方面,VDR 的过表达导致 Snail 的下调,但 E-钙粘蛋白的表达增加,并显著损害细胞形成乳腺球体的能力。与在存在血清的情况下生长的更分化的癌细胞相比,乳腺球体对 1,25-二羟维生素 D(1,25D),即维生素 D 的活性形式的治疗相对不敏感。用一氧化氮(NO)供体 DETA NONOate 处理 H-Ras 转化的 HMLE(HRas)细胞导致 MAP-激酶磷酸酶-1(MKP-1)的诱导和乳腺球体中 ERK1/2 的去磷酸化。用 1,25D 和低浓度的 DETA NONOate 联合处理这些细胞导致乳腺球体的总体大小显著减小,并减少裸鼠中的肿瘤体积。因此,我们的研究结果表明,使用 1,25D 与专门针对 MCSCs 中关键存活途径的药物联合治疗,值得在治疗侵袭性乳腺癌的前瞻性临床试验中进行测试。