RNA binding protein GNL3 up-regulates IL24 and PTN to promote the development of osteoarthritis

发病机制 基因 癌基因 生物 医学 血管生成 骨关节炎 核糖核酸 生物信息学 癌症研究 内科学 病理 遗传学 细胞周期 替代医学
作者
Zhu Zhen,Jun Xie,Upasana Manandhar,Xiaomin Yao,Yawen Bian,Bo Zhang
出处
期刊:Life Sciences [Elsevier]
卷期号:267: 118926-118926 被引量:16
标识
DOI:10.1016/j.lfs.2020.118926
摘要

Osteoarthritis (OA) is a degenerative disease, which has a high incidence in middle-aged and elderly people and tends to occur in weight-bearing or active joints. Current treatment can only relieve symptoms and delay the progression of OA in result of its indistinct pathogenesis. In recent years, more and more studies have focused on the pathogenesis of OA. Nucleolar GTP binding protein 3 (GNL3) is associated with chondrogenic differentiation and can participate in genomic regulation as RNA binding protein (RBP). We used RNA sequencing (RNA-seq) to analyze the overall transcription level of the human cervical cancer cell line HeLa after GNL3 deletion. The results showed that downstream genes IL24 and PTN were down-regulated. IL24 takes part in the progression of OA by inducing articular osteocyte apoptosis, while PTN conducts to the progression of OA by promoting angiogenesis. We validated the results in the human chondrosarcoma cell line SW1353 and OA patients. Compared with the control group, GNL3, IL24 and PTN genes were elevated in OA specimens. This study explored the relationship between GNL3 and these two downstream genes, hoping to find biomarkers in the pathogenesis of osteoarthritis that can be used as therapeutic targets in the future.
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