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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‐1β and TNF‐αtreatment 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. [ABSTRACT FROM AUTHOR]

Gliomas are the commonest and most aggressive primary malignant tumor in the central nervous system. Long noncoding RNAs (lncRNAs) have been identified to act as crucial regulators in multiple biological processes, including tumorigenesis. FAM83H antisense RNA1 (FAM83H‐AS1) has been uncovered to be dysregulated in several cancers. However, the biological role of FAM83H‐AS1 in glioma still needs to be investigated. Currently, our findings indicated that FAM83H‐AS1 was upregulated in glioma tissues and cell lines and high level of FAM83H‐AS1 was associated with poor prognosis of glioma. Loss‐of‐function assays demonstrated that silenced FAM83H‐AS1 obviously suppressed cell proliferation via regulating the cell‐cycle distribution and cell apoptosis rate, and mechanistic experiments revealed that FAM83H‐AS1 could epidemically silence CDKN1A expression through recruiting EZH2 to the promoter of CDKN1A, thereby influencing the cell cycle and proliferation. Collectively, our findings suggested that FAM83H‐AS1 participated in the progression of glioma and might act as a potential therapeutic target and prognosis biomarker for human glioma. [ABSTRACT FROM AUTHOR]