Osteoarthritis (OA) as the most commonly diagnosed joint disease is caused by the breakdown of cartilage in a joint as well as underlying bone [
1]. Osteoarthritis mainly affects elderly and causes chronic pain, resulting in disability [
2]. Due to the direct medical cause and indirect reduction in productivity, OA now is considered as a major economic burden on the modern society [
3]. Pathological changes of OA cannot be reversed. So there is no cure for this disease [
4]. Treatment of OA mainly focuses on pain and symptom relief [
4]. The development of novel anti-OA therapies is mainly limited by the unclear molecular mechanisms of this disease [
5,
6]. Therefore, investigations of the molecular players involved in this disease are of great importance.
Previous studies on the molecular pathogenesis of OA have characterized a considerable number of signaling pathways involved in this disease [
7,
8]. Certain pathways, such as the WNT signaling pathway, have been considered as potential targets for the development of targeted therapies for OA [
7]. Non-coding RNAs (ncRNAs), such as microRNAs (miRNAs) and long (> 200 nt) ncRNAs (lncRNAs) are not involved in protein synthesis but participate in the regulations of human diseases including OA by regulating gene expression [
9]. Certain lncRNAs, such as PVT1, have been proven to participate in OA through multiple ways, such as regulation of cell apoptosis [
10]. However, the roles of most lncRNAs in this disease are still unknown. Small nucleolar RNA host gene 9 (SNHG9), a recently identified lncRNA, has been reported to interact with Wnt2 to participate in glioblastoma [
11]. It has been established that the WNT signaling is a critical player in OA [
7], indicating the potential involvement of SNHG9 in OA. Our preliminary RNA-Seq data revealed the altered expression of SNHG9 in OA and its reverse correlation with miR-34a, which can regulate chondrocyte apoptosis in rat OA model [
12]. This study was therefore carried out to investigate the potential interactions between SNHG9 and miR-34a in OA.