nf - κ b配体受体激活因子(RANKL)在成软骨细胞瘤中表达:可能参与破骨巨细胞募集。

L Huang, Y Y Cheng, L T C Chow, M H Zheng, S M Kumta
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引用次数: 37

摘要

目的:成软骨细胞瘤是一种罕见的,局部侵袭性的骨肿瘤,在受影响骨的骨骺端引起溶骨性破坏。肿瘤细胞可能通过产生nf - κ b配体受体激活因子(RANKL)刺激破骨细胞发生和溶骨破坏,这是调节破骨细胞形成和活性所必需的关键分子。因此,我们研究了RANKL在mRNA和蛋白水平上在成软骨细胞瘤患者肿瘤组织中的表达。方法:采用逆转录聚合酶链反应(RT-PCR)分析RANKL基因转录本的表达,采用原位杂交和免疫组织化学方法证实RANKL mRNA和蛋白的细胞定位。结果:RT-PCR分析显示,RANKL mRNA存在于所有成软骨细胞瘤标本和正常松质骨标本中,而不存在于正常关节软骨和软骨肉瘤组织中。相反,RANKL的诱饵受体骨保护素(OPG)的基因转录本在所有类型的组织中都被检测到。S-100免疫组化染色阳性证实了成软骨细胞瘤中单个核细胞的软骨样起源。RANKL mRNA和蛋白均在这些肿瘤单核细胞中表达。结论:这些发现提示RANKL可能参与了成软骨细胞瘤肿瘤细胞诱导的破骨细胞样细胞募集和随后的溶骨性骨破坏。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Receptor activator of NF-kappaB ligand (RANKL) is expressed in chondroblastoma: possible involvement in osteoclastic giant cell recruitment.

Aims: Chondroblastoma is a rare, locally aggressive bone tumour that causes osteolytic destruction at the epiphyseal end of the affected bone. It is possible that tumour cells may stimulate osteoclastogenesis and osteolytic destruction through the production of receptor activator of NF-kappaB ligand (RANKL), which is a key molecule essential for regulating osteoclast formation and activity. Therefore, the expression of RANKL at both the mRNA and the protein level was investigated in chondroblastoma tumour tissue obtained from patients.

Methods: The expression of RANKL gene transcripts was analysed by the reverse transcription-polymerase chain reaction (RT-PCR), and the cellular localisation of RANKL mRNA and protein was demonstrated by means of in situ hybridisation and immunohistochemistry.

Results: RT-PCR analysis indicated that RANKL mRNA was present in all chondroblastoma specimens and normal cancellous bone samples, but not in normal articular cartilage and chondrosarcoma tissues. In contrast, gene transcripts of osteoprotegerin (OPG), the decoy receptor of RANKL, were detected in all types of tissues. The chondroid origin of neoplastic mononuclear cells in chondroblastoma was confirmed by positive S-100 immunohistochemical staining. Both RANKL mRNA and protein were exclusively expressed in these neoplastic mononuclear cells.

Conclusions: These findings suggest that RANKL may be involved in the tumour cell induced recruitment of osteoclast-like cells and consequent osteolytic bone destruction in chondroblastoma.

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