环状 RNA FAM169A 作为竞争性内源性 RNA，通过靶向 miR-583 和 BTRC 调节椎间盘退变。
The circular RNA FAM169A functions as a competitive endogenous RNA and regulates intervertebral disc degeneration by targeting miR-583 and BTRC.
机构信息
Department of Orthopaedics, Hebei Province Cangzhou Hospital of Integrated Traditional and Western Medicine (Cangzhou No. 2 Hospital), 31 Huanghe Road, Cangzhou, 061001, Hebei, PR China.
Department of Breast Surgery, Hebei Province Cangzhou Hospital of Integrated Traditional and Western Medicine (Cangzhou No. 2 Hospital), 31 Huanghe Road, Cangzhou, 061001, Hebei, PR China.
出版信息
Cell Death Dis. 2020 May 4;11(5):315. 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.
椎间盘退变（IDD）是导致下腰痛的重要因素，但其潜在机制仍知之甚少。在本研究中，我们研究了环状 RNA FAM169A（circ-FAM169A）在退变髓核（NP）组织中的作用，并在培养的人 NP 细胞中验证了其功能。NP 细胞中 circ-FAM169A 的过表达显著增强了 NP 细胞中细胞外基质（ECM）的分解代谢，同时抑制了 ECM 的合成代谢。此外，circ-FAM169A 可与 miR-583 结合，后者可能上调 NF-κB 信号通路的诱导剂 BTRC。总之，本研究表明，circ-FAM169A 通过 miR-583/BTRC 信号通路促进 IDD 的发展。这些发现为 IDD 的治疗提供了一种潜在的治疗选择。
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