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Ginsenoside Rb1 (GRb1), a major ingredient of ginseng, has been found to be a potential protective agent in spinal cord injury (SCI) and in activated microglia‐induced neuronal injury. This study discovered that GRb1 could facilitate miR‐130b‐5p expression in SCI rats and Toll‐like receptor 4 (TLR4; a crucial player in inflammation) was a potential target of miR‐130b‐5p. Hence, we further investigated whether GRb1 could relieve SCI by reducing microglia‐mediated inflammatory responses and neuronal injury via miR‐130b‐5p/TLR4 pathways. The results showed that GRb1 alleviated SCI through inhibiting neuronal apoptosis and proinflammatory factor expression via increasing miR‐130b‐5p.GRb1 weakened the damage of activated microglia to neurons through upregulating miR‐130b‐5p. miR‐130b‐5p attenuated activated microglia‐induced neuron injury via targeting TLR4. GRb1 inactivated TLR4/nuclear factor‐κB (NF‐κB) activation and inhibited proinflammatory cytokine secretion by increasing miR‐130b‐5p in activated microglia. As a conclusion, GRb1 alleviated SCI through reducing activated microglia‐induced neuronal injury via miR‐130b‐5p/TLR4/NF‐κB axis, providing a deep insight into the molecular basis of GRb1 in the treatment of SCI. [ABSTRACT FROM AUTHOR]

A growing amount of evidence has shown that long noncoding RNAs (lncRNAs) play crucial roles in osteosarcoma (OS). However, little knowledge is available about the functional roles and molecular mechanisms of lncRNA Alu‐mediated p21 transcriptional regulator (APTR) in OS. Herein, APTR expression was demonstrated to be significantly upregulated in OS tumor tissues and four OS cell lines (including MG63, 143B, Saos‐2, and HOS) compared with the adjacent tissues and human osteoblast cell line hFOB1.19, respectively. We confirmed miR‐132‐3p to be a target for APTR, and its expression was demonstrated to be inhibited by APTR. In functional terms, knockdown of APTR and overexpression of miR‐132‐3p both, remarkably repressed human OS cell proliferation, invasion and migration, and induced apoptosis. Also, Yes‐associated protein 1 (YAP1) was determined as an inhibitory target of miR‐132‐3p. Moreover, our findings demonstrated that the repression of YAP1 protein expression and the suppression of Ki‐67, MMP9, and Bcl2 expression induced by APTR knockdown required increased miR‐132‐3p. Thus, APTR contributed to OS progression through repression of miR‐132‐3p and upregulation of YAP1 expression. Therefore, we have uncovered a novel regulatory mechanism by which the APTR/miR‐132‐3p/YAP1 axis can regulate OS progression. In summary, our study was the first to establish that Alu‐mediated p21 transcriptional regulator (APTR) can function as an oncogenic long noncoding RNA in osteosarcoma (OS). Most importantly, we explored a new regulatory mechanism of the APTR/miR‐132‐3p/Yes‐associated protein 1 axis in the regulation of OS cells, which could be a potential therapeutic biomarker for OS. [ABSTRACT FROM AUTHOR]