LncRNA FAM83H-AS1 induces nucleus pulposus cell growth via targeting the Notch signaling pathway.

Long noncoding RNA (lncRNA) represents a new group of transcripts which act a critical role in various biological and pathological processes. Growing evidence suggested that a new lncRNA, FAM83H-AS1, played important roles in several cancers. However, the underlying mechanisms of FAM83H-AS1-regulating functions in intervertebral disc degeneration (IDD) have yet to be explained. Thus study examined the role of lncRNA FAM83H-AS1 in progression of IDD. First, we proved that expression level of FAM83H-AS1 was expressed in nondegenerated nucleus pulposus (NP) tissues and degenerative NP samples. Moreover, we studied the expression level of FAM83H-AS1 relationship of the clinical disc degeneration grade. Our data suggested that FAM83H-AS1 expression was downregulated in normal NP samples compared with in the degenerated NP samples. FAM83H-AS1 expression was positively correlated with degree of disc degeneration grade. The expression of FAM83H-AS1 was positively correlated with scores of Pfirrmann grade. FAM83H-AS1 expression was increased by IL-1 beta and TNF-alpha treatment in NP cells. Ectopic expression of FAM83H-AS1 induced cell growth and modulated extracellular matrix (ECM) expression in the NP cell. Elevated expression of FAM83H-AS1 promoted Notch1 and Hes1 expression in NP cells. Furthermore, FAM83H-AS1 induced NP cell growth and modulated ECM expression through targeting Notch 1. To conclude, dysregulated expression of FAM83H-AS1 played a crucial role in progression of IDD.