Corey Eva, Brown Lisha G, Kiefer Jeffrey A, Quinn Janna E, Pitts Tiffany E M, Blair Julie M, Vessella Robert L
Department of Urology, University of Washington, Seattle, Washington 98195, USA.
Cancer Res. 2005 Mar 1;65(5):1710-8. doi: 10.1158/0008-5472.CAN-04-2033.
Osteoprotegerin (OPG), a critical regulator of osteoclastogenesis, is expressed by prostate cancer cells, and OPG levels are increased in patients with prostate cancer bone metastases. The objective of this study was to investigate the effects of OPG overexpression on prostate cancer cells and prostate cancer/bone cell interactions in vitro and in vivo. OPG-transfected C4-2 cells expressed 8.0 ng OPG per mL per 10(6) cells, whereas no OPG was detected in the media of C4-2 cells transfected with a control plasmid. OPG overexpressed by C4-2 cells protected these cells from tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis and decreased osteoclast formation. Subcutaneous OPG-C4-2 and pcDNA-C4-2 tumors exhibited similar growth and take-rate characteristics. However, when grown in bone, tumor volume was decreased in OPG-C4-2 versus pcDNA-C4-2 (P=0.0017). OPG expressed by C4-2 cells caused increases in bone mineral density (P=0.0074) and percentage of trabecular bone volume (P=0.007), and decreases in numbers of osteoblasts and osteoclasts when compared with intratibial pcDNA-C4-2 tumors (P=0.003 and P=0.019, respectively). In summary, our data show that increased expression of OPG in C4-2 cells does not directly affect proliferation of prostate cancer cells but indirectly decreases growth of C4-2 tumors in the bone environment. Our data also show that OPG expressed by C4-2 cells inhibits bone lysis associated with C4-2 bone metastasis, which results in net increases in bone volume. We therefore hypothesize that OPG expressed in prostate cancer patient bone metastases may be at least partially responsible for the osteoblastic character of most prostate cancer bone lesions.
骨保护素(OPG)是破骨细胞生成的关键调节因子,由前列腺癌细胞表达,且在前列腺癌骨转移患者中OPG水平升高。本研究的目的是在体外和体内研究OPG过表达对前列腺癌细胞以及前列腺癌/骨细胞相互作用的影响。转染OPG的C4-2细胞每10⁶个细胞每毫升表达8.0纳克OPG,而转染对照质粒的C4-2细胞培养基中未检测到OPG。C4-2细胞过表达的OPG保护这些细胞免受肿瘤坏死因子相关凋亡诱导配体诱导的凋亡,并减少破骨细胞形成。皮下接种的OPG-C4-2和pcDNA-C4-2肿瘤表现出相似的生长和接种率特征。然而,当在骨中生长时,与pcDNA-C4-2相比,OPG-C4-2的肿瘤体积减小(P = 0.0017)。与胫骨内接种pcDNA-C4-2肿瘤相比,C4-2细胞表达的OPG导致骨矿物质密度增加(P = 0.0074)和骨小梁体积百分比增加(P = 0.007),而成骨细胞和破骨细胞数量减少(分别为P = 0.003和P = 0.019)。总之,我们的数据表明,C4-2细胞中OPG表达增加并不直接影响前列腺癌细胞的增殖,但间接减少了C4-2肿瘤在骨环境中的生长。我们的数据还表明,C4-2细胞表达的OPG抑制与C4-2骨转移相关的骨溶解,这导致骨体积净增加。因此,我们假设前列腺癌患者骨转移中表达的OPG可能至少部分地导致了大多数前列腺癌骨病变的成骨细胞特征。