Long non‑coding RNA FAF1 promotes intervertebral disc degeneration by targeting the Erk signaling pathway.

Abstract

Intervertebral disc degeneration (IDD) has become the most common cause of low‑back pain, and it imposes a heavy burden on patients with IDD and society. The effects of long non‑coding RNAs on the proliferation and development of IDD have attracted increasing attention. The present study aimed to investigate the role and molecular mechanism of Fas‑associated protein factor‑1 (FAF1) in IDD. The expression of FAF1 was detected by reverse transcription‑quantitative polymerase chain reaction. CCK‑8 and immunofluorescence staining were used to determine cell proliferation. Flow cytometry was performed to measure the cell cycle and apoptosis. Western blotting was used to test p‑Erk expression. The results of the present study demonstrated that the expression of FAF1 was upregulated in patients with disc bulging, herniation and IDD, and the expression of FAF1 was positively correlated with the grade of disc degeneration according to the patients' Pfirrmann score. The overexpression of FAF1 in nucleus pulposus (NP) cells promoted cell proliferation by increasing the percentage of cells in the S‑phase of the cell cycle. The expression of phosphorylated extracellular signal‑regulated kinase (Erk), a possible target of FAF1, was consistent with the expression of FAF1. In addition, it was elucidated that inactivation of the Erk signaling pathway by PD98059 reversed the effect of FAF1 on NP cell proliferation. Taken together, these results demonstrated that FAF1 was vital in the proliferation of NP cells by modulating the Erk signaling pathway, which suggests that FAF1 may be a novel marker in the early diagnosis of IDD and a therapeutic target for patients.