Effects of IGFBP3 gene silencing mediated inhibition of ERK/MAPK signaling pathway on proliferation, apoptosis, autophagy, and cell senescence in rats nucleus pulposus cells.

OBJECTIVE:Disc degeneration is the common life-threatening disease characterized by flank pain. The gene expression of insulin-like growth factor binding protein 3 (IGFBP3) is increased in patients with disc degeneration, however, its mechanism is still unknown. This study aimed to investigate the influence of IGFBP3 gene silencing mediated inhibition of extracellular signal-related kinase (ERK)/mitogen-activated protein kinase (MAPK) signaling on proliferation, apoptosis, autophagy, and cell senescence in rats nucleus pulposus (NP) cells. METHODS:The expression of IGFBP3 in disc NP of patients was assessed by real-time PCR (RT-PCR) and western blot. RT-PCR, transwell assay, immunohistochemical staining, SA-β-Gal staining, and western blot were performed to explore the molecular mechanism of IGFBP3 in NP cell migration and invasion. RESULTS:In this study, IGFBP3 was highly expressed in disc NP of patients. With RT-PCR, transwell assay, immunohistochemical staining, SA-β-Gal staining, and western blot, downregulated IGFBP3 could inhibit NP cells' migration and invasion by targeting the ERK/MAPK signaling pathway. CONCLUSION:Our findings revealed that the inhibition of the ERK/MAPK pathway was mediated by IGFBP3 silencing that had effects on proliferation, apoptosis, autophagy, and cell senescence. Furthermore, our findings suggested the underlying mechanism of disc degeneration.

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