The circular RNA FAM169A functions as a competitive endogenous RNA and regulates intervertebral disc degeneration by targeting miR-583 and BTRC

• Published in: Cell death & disease Vol. 11; no. 5; p. 315
• Main Authors: Guo, Wei, Mu, Kun, Zhang, Bin, Sun, Chao, Zhao, Ling, Dong, Zhan-Yin, Cui, Qing
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 04.05.2020; Springer Nature B.V
• Subjects: 13/89; 14/32; 38/39; 42/44; 631/80; 692/699; Adult; Animals; Antibodies; Base Sequence; beta-Transducin Repeat-Containing Proteins - metabolism; Biochemistry; Biomedical and Life Sciences; Cell Biology; Cell Culture; Circular RNA; Degeneration; Degenerative disc disease; Disease Models, Animal; Extracellular matrix; Extracellular Matrix - metabolism; Female; Gene Expression Profiling; Gene Silencing; Humans; Immunology; Intervertebral Disc Degeneration - diagnostic imaging; Intervertebral Disc Degeneration - genetics; Intervertebral discs; Life Sciences; Low back pain; Male; MicroRNAs - genetics; MicroRNAs - metabolism; NF-κB protein; Nucleus pulposus; Nucleus Pulposus - metabolism; Nucleus Pulposus - pathology; Principal Component Analysis; Rats, Sprague-Dawley; Ribonucleic acid; RNA; RNA, Circular - genetics; RNA, Circular - metabolism; Signal Transduction; Up-Regulation - genetics
• ISSN: 2041-4889; 2041-4889
• DOI: 10.1038/s41419-020-2543-8

Intervertebral disc degeneration (IDD) is an important factor leading to low back pain, although the underlying mechanisms remain poorly understood. In this study we examined the role of circular RNA FAM169A (circ-FAM169A) in degenerative nucleus pulposus (NP) tissues, and validated its function in cultured human NP cells. Overexpression of circ-FAM169A in NP cells markedly enhanced extracellular matrix (ECM) catabolism and suppressed ECM anabolism in NP cells. Furthermore, circ-FAM169A sequestered miR-583, which could potentially upregulate BTRC, an inducer of the NF-κB signaling pathway. In conclusion, the present study revealed that circ-FAM169A promotes IDD development via miR-583/BTRC signaling. These findings provide a potential therapeutic option for the treatment of IDD.