Chen Tai C, Holick Michael F, Lokeshwar Bal L, Burnstein Kerry L, Schwartz Gary G
Department of Medicine, Endocrine Section, Boston University School of Medicine, 715 Albany Street, Boston, MA 02118, USA.
Recent Results Cancer Res. 2003;164:273-88. doi: 10.1007/978-3-642-55580-0_20.
Prostate cancer cells contain specific receptors (VDR) for la,25-dihydroxyvitamin D (1alpha,25(OH)2D), which is known to inhibit the proliferation and invasiveness of these cells. These findings support the use of 1alph,25(OH)2D for prostate cancer therapy. However, because 1alpha,25(OH)2D can cause hypercalcemia, analogs of 1alpha,25(OH)2D that are less calcemic but which exhibit potent antiproliferative activity would be attractive as therapeutic agents. We studied four vitamin D compounds: 25-hydroxyvitaminD3 [25(OH)D3], which is converted to 1alpha,25(OH)2D3 in prostate cells, and three analogs of 1alpha,25(OH)2D3: EB1089, 19-nor-1alpha,25(OH)2D2 and hexafluoro-1alpha,25(OH)2D3 (F6-1alpha,25(OH)2D3). 19-nor-1alpha,25(OH)2D2 has been shown to be less calcemic than 1alpha,25(OH)2D3 in clinical trials. F6-1alpha,25(OH)2D3 has been shown to be 100-fold more active than 1alpha,25(OH)2D3 and to be longer-lasting in inhibiting keratinocyte proliferation in vitro. EB1089 has been shown to be less calcemic than 1alpha,25(OH)2D3 in rats implanted with Leydig cell tumors. For 25(OH)D3, 19-nor-1alpha,25(OH)2D2 and F6-1alpha,25(OH)2D3, we studied the in vitro effects and compared their activity to 1alpha,25(OH)2D3 on cellular proliferation by 3H-thymidine incorporation assay. In addition, we studied transactivation of the VDR in the presence of 25(OH)D3 and 19-nor-1alpha,25(OH)2D2 in prostate cells. For EB1089, we compared its inhibition of prostate cancer metastasis to that induced by 1alpha,25(OH)2D3 in vivo in the rat Dunning MAT LyLu prostate cancer model. We found that 1alpha,25(OH)2D3 and 19-nor-1alpha,25(OH)2D2 caused similar dose-dependent inhibition in 3H-thymidine incorporation into DNA in prostate cells and behaved similarly in the CAT reporter gene transactivation assay in PC-3/VDR cells. F6-1alpha,25(OH)2D3 is 10- to 50-fold more active than 1alpha,25(OH)2D3 in 3H-thymidine incorporation into DNA in the primary cultured prostate cells. Likewise, 25(OH)D3 had comparable antiproliferative activity to la,25(OH)2D3. In the rat model, tumor volumes and the number of metastases in the lungs were significantly reduced by both 1alpha,25(OH)2D3 (10.4 +/- 2.81 tumor foci) and EB1089 (7.7+/-1.29 tumor foci) compared to controls (22.7 +/- 1.98 tumor foci). Although serum calcium levels were significantly elevated in both 1alph,25(OH)2D3- and EB1089-treated rats, EB1089 was significantly less calcemic than 1alpha,25(OH)2D3 (12.59+/-0.21 mg/dl versus 14.47+/-.46 mg/dL; 1 microg/kg; p < 0.001). In conclusion, our data indicate that 25(OH)D3 and the three 1alpha,25(OH)2D analogs represent two different solutions to the problem of hypercalcemia associated with vitamin D-based prostate cancer therapies: 25(OH)D3 requires the presence of 25-hydroxyvitaminD-1alpha-hydroxylase, whereas 19-nor-1alpha,25(OH)2D2, F6-1alpha,25(OH)2D3 and EB1089 do not. These compounds may be good candidates for human clinical trials in prostate cancer.
前列腺癌细胞含有1,25 - 二羟基维生素D(1α,25(OH)2D)的特异性受体(VDR),已知该物质可抑制这些细胞的增殖和侵袭性。这些发现支持将1α,25(OH)2D用于前列腺癌治疗。然而,由于1α,25(OH)2D可导致高钙血症,那么钙血症较低但具有强大抗增殖活性的1α,25(OH)2D类似物作为治疗药物将具有吸引力。我们研究了四种维生素D化合物:25 - 羟基维生素D3 [25(OH)D3],其在前列腺细胞中可转化为1α,25(OH)2D3,以及1α,25(OH)2D3的三种类似物:EB1089、19 - 去甲 - 1α,25(OH)2D2和六氟 - 1α,25(OH)2D3(F6 - 1α,25(OH)2D3)。在临床试验中,已证明19 - 去甲 - 1α,25(OH)2D2的钙血症低于1α,25(OH)2D3。F6 - 1α,25(OH)2D3已被证明比1α,25(OH)2D3活性高100倍,且在体外抑制角质形成细胞增殖的作用更持久。在植入睾丸间质细胞瘤的大鼠中,已证明EB1089的钙血症低于1α,25(OH)2D3。对于25(OH)D3、19 - 去甲 - 1α,25(OH)2D2和F6 - 1α,25(OH)2D3,我们研究了它们的体外作用,并通过3H - 胸腺嘧啶核苷掺入试验将其活性与1α,25(OH)2D3对细胞增殖的作用进行比较。此外,我们研究了在前列腺细胞中25(OH)D3和19 - 去甲 - 1α,25(OH)2D2存在时VDR的反式激活。对于EB1089,我们在大鼠Dunning MAT LyLu前列腺癌模型中比较了其对前列腺癌转移的抑制作用与1α,25(OH)2D3诱导的抑制作用。我们发现,1α,25(OH)2D3和19 - 去甲 - 1α,25(OH)2D2在前列腺细胞中对3H - 胸腺嘧啶核苷掺入DNA具有相似的剂量依赖性抑制作用,并且在PC - 3/VDR细胞的CAT报告基因反式激活试验中的表现相似。在原代培养的前列腺细胞中,F6 - 1α,25(OH)2D3在3H - 胸腺嘧啶核苷掺入DNA方面的活性比1α,25(OH)2D3高10至50倍。同样,25(OH)D3具有与1α,25(OH)2D3相当的抗增殖活性。在大鼠模型中,与对照组(22.7±1.98个肿瘤灶)相比,1α,25(OH)2D3(10.4±2.81个肿瘤灶)和EB1089(7.7±1.29个肿瘤灶)均显著降低了肿瘤体积和肺转移灶数量。虽然在接受1α,25(OH)2D3和EB1089治疗的大鼠中血清钙水平均显著升高,但EB1089的钙血症明显低于1α,25(OH)2D3(12.59±0.21mg/dl对14.47±0.46mg/dL;1μg/kg;p<0.001)。总之,我们的数据表明,25(OH)D3和三种1α,25(OH)2D类似物代表了与基于维生素D的前列腺癌治疗相关的高钙血症问题的两种不同解决方案:25(OH)D3需要25 - 羟基维生素D - 1α - 羟化酶的存在,而19 - 去甲 - 1α,25(OH)2D2、F6 - 1α,25(OH)2D3和EB1089则不需要。这些化合物可能是前列腺癌人体临床试验的良好候选药物。