MiR-874-3p suppresses TNF-α-induced inflammation in adipocytes by targeting nucleolin.
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Many investigations have indicated the significance of microRNAs (miRNAs) as potential biomarkers for early obesity in children. MiR-874-3p was revealed to be downregulated in overweight/obese children. However, the specific function and mechanism of miR-874-3p in the progression of childhood obesity remain unclear. Human Simpson-Golabi-Behmel syndrome (SGBS) adipocytes were stimulated with tumor necrosis factor α (TNF-α) to establish an in vitro cell model. CCK-8 assay and ELISA were used to assess cell viability and proinflammatory cytokine secretion, respectively. RT-qPCR was used for miR-874-3p expression analysis. Western blotting was utilized to evaluate protein levels of miR-874-3p downstream targets and nuclear factor kappa B (NF-κB) signaling-related markers. Luciferase reporter assay was conducted to verify the binding relation between miR-874-3p and nucleolin (NCL). MiR-874-3p overexpression attenuated TNF-α-induced inhibition of cell viability and promotion of proinflammatory cytokine production. Mechanistically, NCL served as a target of miR-874-3p, and overexpressing miR-874-3p inactivated NCL-mediated NF-κB signaling. Moreover, NCL upregulation reversed miR-874-3p overexpression-mediated effects on the viability and proinflammatory cytokines in SGBS adipocytes. MiR-874-3p alleviates TNF-α-induced inflammatory response in SGBS adipocytes by downregulating NCL and inactivating NF-κB signaling.