Long noncoding RNAs (lncRNAs) get great involvements in the development of countless cancers. Nonetheless, the deep molecular mechanism by which lncRNA regulates the formation of glioma is unclear. In our study, the expression of PSMB8-AS1 was dramatically upregulated in glioma tissues and cells, further, PSMB8-AS1 silencing restrained cell proliferation in glioma, and the results of PSMB8-AS1 overexpression were opposite. Moreover, PSMB8-AS1 could bind with miR-574-5p, which was low expressed in glioma cells. In addition, RAB10 acted the target gene of miR-574-5p, and PSMB8-AS1 could regulate RAB10 via modulating miR-574-5p. Besides, miR-574-5p inhibitor/mimics remedied the repressive/simulative role of PSMB8-AS1 depletion/overexpression, and RAB10 downregulation/upregulation reversed the encouraging/blocked function caused by miR-574-5p inhibitor/mimics in PSMB8-AS1 depletion/overexpression transfected glioma cells. Additionally, ELK1, a transcription factor, could active PSMB8-AS1 expression. To be concluded, PSMB8-AS1 activated by ELK1 promotes cell proliferation in glioma via regulating miR-574-5p/RAB10, which may be contributory to find new targets to treat glioma.

Studies have revealed the aberrant expression of lncRNAs is responsible for human carcinogenesis. MIR4697 host gene (MIR4697HG) is an upregulated lncRNA that promoted cell growth and metastasis in other cancers. In this study, we tested the expression of MIR4697HG in glioma cells and detected the comparatively down-regulated expression. RAD1 is an upstream regulator for MIR4697HG. This study aimed at exploring the regulatory mechanism and function of RAD1/MIR4697HG/PRR12 axis in glioma. We profiled the expression of MIR4697HG in glioblastoma multiforme (GBM) tissues according to GEPIA database as well as in glioma cells by qPCR. Functional experiments confirmed relevant role of MIR4697HG in regulating glioma cell proliferation and migration. We also carried out luciferase reporter assay, pull down assay and RIP assay to verify the location and interaction among the indicated RNA molecules. The expression of MIR4697HG is down-regulated significantly in glioma cells due to the up-regulated expression of RAD21. MiR-766-5p was identified functioning as a sponge for MIR4697HG and is sequestered by MIR4697HG. We also found either miR-766-5p inhibitor or PRR12 knockdown rescued the function depletion caused by MIR4697HG overexpression. In all, the down-regulated expression of MIR4697HG inhibited PRR12 to suppress glioma and led to the deterioration of glioma. RAD21-induced down-regulated expression of MIR4697HG is correlated with aggravation of glioma. The MIR4697HG/miR-766-5p/PRR12 axis predicts poor results in glioma and MIR4697HG could be considered as a promising biomarker for diagnosis and treatment of glioma.

Background: Intracerebral hemorrhage (ICH) remains a devastating neurological disorder with limited therapeutic options. Neural stem cell (NSC)‐based therapies have emerged as a potential regenerative approach, yet the molecular mechanisms regulating NSC behavior require further elucidation. The role of miR‐21 in NSC differentiation and proliferation during ICH recovery remains unexplored. Methods: In vitro NSC cultures were analyzed for miR‐21 expression dynamics during differentiation via qPCR. Lentiviral overexpression and knockdown of miR‐21 were employed to assess its functional impact. The SOX2/LIN28‐let‐7 pathway was investigated using Western blot, luciferase reporter assays, and immunofluorescence. In vivo, miR‐21‐overexpressing NSCs were transplanted into a murine ICH model, with neurogenesis evaluated by immunostaining and neurological recovery assessed through behavioral tests (mNSS, rotarod). Results: miR‐21 expression significantly increased during NSC differentiation, correlating with reduced SOX2 levels. Mechanistically, miR‐21 directly targeted SOX2, disrupting the SOX2/LIN28‐let‐7 axis to promote NSC proliferation and lineage commitment. In ICH mice, transplantation of miR‐21‐overexpressing NSCs enhanced neurogenesis and improved motor coordination and neurological deficits at 28 days post‐transplantation. Conclusions: Our findings identify miR‐21 as a critical regulator of NSC plasticity through SOX2/LIN28‐let‐7 signaling, highlighting its therapeutic potential for enhancing neuroregeneration and functional recovery in ICH. Targeting miR‐21 may represent a novel strategy to optimize NSC‐based therapies for hemorrhagic stroke.