Beaudin Sarah G, Robilotto Samantha, Welsh JoEllen
Cancer Research Center, Rensselaer, NY 12144, United States; Department of Biomedical Sciences, Rensselaer, NY 12144, United States.
Cancer Research Center, Rensselaer, NY 12144, United States.
J Steroid Biochem Mol Biol. 2015 Apr;148:96-102. doi: 10.1016/j.jsbmb.2014.09.014. Epub 2014 Sep 18.
Previous genomic profiling of immortalized, non-tumorigenic human breast epithelial cells identified a set of 1,25-dihydroxyvitamin D3 (1,25D) regulated genes with potential relevance to breast cancer prevention. In this report, we characterized the effect of 1,25D on a subset of these genes in six cell lines derived from mammary tissue and breast cancers. Non-tumorigenic cell lines included hTERT-HME1, HME and MCF10A cells which are often used to model normal breast epithelial cells. Breast cancer cell lines included MCF7 cells (a model of early stage, estrogen-dependent disease), DCIS.com cells (a derivative of MCF10A cells that models in situ breast cancer) and Hs578T cells (a model of metastatic disease). All of these cell lines express the vitamin D receptor (VDR) and exhibit anti-cancer responses to 1,25D such as changes in proliferation, apoptosis, metabolism, or invasion. Our comparative data demonstrate highly variable responses to 1,25D (100nM, 24h) between the cell lines. In both hTERT-HME1 and HME cell lines, CYP24A1, SLC1A1 and ITGB3 were up-regulated whereas KDR, GLUL and BIRC3 were down-regulated in response to 1,25D. In contrast, no changes in SLC1A1, ITGB3 or GLUL expression were detected in 1,25D treated MCF10A cells although KDR and BIRC3 were down-regulated by 1,25D. The effects of 1,25D on these genes in the breast cancer cell lines were blunted, with the DCIS.com cells exhibiting the most similar responses to the immortalized hTERT-HME1 and HME cells. The differences in cellular responses were not due to general impairment in VDR function as robust CYP24A1 induction was observed in all cell lines. Thus, our data indicate that the genomic changes induced by 1,25D are highly cell-type specific even in model cell lines derived from the same tissue. The implication of these findings is that genomic responses to changes in vitamin D status in vivo are likely to be distinct from individual to individual, particularly in neoplastic tissue. This article is part of a Special Issue entitled '17th Vitamin D Workshop'.
先前对永生化、无致瘤性的人乳腺上皮细胞进行的基因组分析,确定了一组1,25 - 二羟基维生素D3(1,25D)调控的基因,这些基因可能与乳腺癌预防相关。在本报告中,我们描述了1,25D对源自乳腺组织和乳腺癌的六种细胞系中这些基因的一个子集的影响。非致瘤性细胞系包括hTERT - HME1、HME和MCF10A细胞,它们常被用于模拟正常乳腺上皮细胞。乳腺癌细胞系包括MCF7细胞(早期雌激素依赖性疾病模型)、DCIS.com细胞(MCF10A细胞的衍生物,用于模拟原位乳腺癌)和Hs578T细胞(转移性疾病模型)。所有这些细胞系都表达维生素D受体(VDR),并对1,25D表现出抗癌反应,如增殖、凋亡、代谢或侵袭的变化。我们的比较数据表明,各细胞系对1,25D(100nM,24小时)的反应差异很大。在hTERT - HME1和HME细胞系中,CYP24A1、SLC1A1和ITGB3上调,而KDR、GLUL和BIRC3则因1,25D而下调。相比之下,在1,25D处理的MCF10A细胞中未检测到SLC1A1、ITGB3或GLUL表达的变化,尽管KDR和BIRC3因1,25D而下调。1,25D对乳腺癌细胞系中这些基因的影响减弱,DCIS.com细胞表现出与永生化的hTERT - HME1和HME细胞最相似的反应。细胞反应的差异并非由于VDR功能的普遍受损,因为在所有细胞系中都观察到了强烈的CYP24A1诱导。因此,我们的数据表明,即使在源自同一组织的模型细胞系中,1,25D诱导的基因组变化也是高度细胞类型特异性的。这些发现的意义在于,体内对维生素D状态变化的基因组反应可能因人而异,尤其是在肿瘤组织中。本文是名为“第17届维生素D研讨会”的特刊的一部分。