Downregulation of NKD1 in human osteosarcoma and its clinical significance

NKD1在人骨肉瘤中的下调及其临床意义

阅读:4
作者:Xiang Chen, Ping Xu, Jianwei Zhu, Fan Liu

Abstract

Naked cuticle homolog 1 (NKD1), a negative modulator of the canonical Wnt/β‑catenin pathway, is expressed in multiple normal tissues. However, there is little information regarding NKD1 expression in osteosarcoma. The aim of the present study was to explore the expression and clinicopathological significance of NKD1 in human osteosarcoma. In the present study, NKD1 protein and mRNA expression levels were detected by western blotting and reverse transcription‑quantitative polymerase chain reaction, respectively. The results revealed that NKD1 expression levels were significantly lower in osteosarcoma tissues compared with normal bone tissue, and were significantly lower in patients with lung metastasis compared with patients without lung metastasis. In addition, with increasing Enneking stage, the NKD1 expression levels decreased. These data indicated that reduction of NKD1 may be associated with carcinogenesis, lung metastasis and Enneking stage in osteosarcoma. This interpretation is consistent with the results obtained from experiments on MG63 osteosarcoma cells in vitro. In order to explore the function of NKD1 in osteosarcoma, the expression of NKD1 in the human osteosarcoma MG‑63 cell line was upregulated by transfection with an adenovirus containing an NKD1 vector. The results revealed that upregulation of NKD1 expression reduced the proliferation and migration of osteosarcoma cells by inhibiting expression of β‑catenin, cyclin D1 and MMP‑9 protein. These data suggested that the downregulation of NKD1 may be involved in the proliferation and migration of osteosarcoma cells through the activation of the canonical Wnt signaling pathway, and it may be a potential prognostic marker and therapeutic target for patients with osteosarcoma.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。