The aim of the present study was to investigate the effect of microRNA (miR)-34a on spinal cord injury (SCI)-induced inflammation and the possible underlying mechanisms. The results indicated that miR-34a expression was downregulated in a rat model of SCI compared with the control group. Furthermore, miR-34a knockdown was demonstrated to aggravate inflammation, inhibit cell proliferation and enhance apoptosis in an in vitro model of SCI. MiR-34a inhibition was demonstrated to upregulate the expression of inducible nitric oxide synthase and nitric oxide, as well as inducing the expression of toll-like receptor 4 (TLR4) and high mobility group box-1 (HMGB-1) in an in vitro model of SCI. TLR4 inhibitor reduced the effects of miR-34a downregulation on inflammation and cell growth in SCI. Together, these results suggest that miR-34a is able to alleviate SCI via inhibiting HMGB-1 expression in TLR4 signaling.
Background As a skeletal malignancy, osteosarcoma has high incidence among primary malignant bone tumors. With increasing researches on molecules which mediate cancer progression, molecular mechanism has gradually become the pivot of osteosarcoma research and treatment. Aim Our study aimed at investigating the function of G3BP stress granule assembly factor 2 (G3BP2), which is an oncogene for breast cancer (BC) and prostate cancer but remains unknown in osteosarcoma cells. Methods Related gene expression was confirmed by RT-qPCR. Functional assays including immunofluorescence (IF), colony formation, transferase-mediated dUTP nick-end labeling (TUNEL) as well as transwell assays were utilized to test the cell biological process caused by the genes. Meanwhile, RNA pull-down assay, along with luciferase reporter and RNA immunoprecipitation (RIP) assays, was utilized to detect the interaction G3BP2, miR-124-3p and FGD5 antisense RNA 1 (FGD5-AS1) may exert on the regulation of osteosarcoma cells. Results G3BP2 was with high expression in osteosarcoma cells, and it aggravated the malignant cell behaviors in osteosarcoma. Additionally, miR-124-3p was verified to negatively regulate G3BP2 expression in osteosarcoma cells. Moreover, lncRNA FGD5-AS1 was predicted and testified to be the sponge of miR-124-3p and modulated G3BP2 expression positively. Subsequently, FGA5-AS1 accelerated osteosarcoma cell proliferation through up-regulating G3BP2. Furthermore, we identified EBF transcription factor 1 (EBF1) as the transcription factor for FGA5-AS1, and EBF1 served as a tumor facilitator in osteosarcoma cells. Conclusion EBF1 induced-FGA5-AS1 aggravated osteosarcoma cell malignancy by targeting miR-124-3p and G3BP2.
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