Abstract Background Glioma is a brain tumor with high morbidity and mortality rates.Understanding its molecular pathogenesis can provide targets and therapeutic strategies for glioma treatment.miR-338-3p represses tumor Sieves growth in several cancers, including glioma.Thus, this study aimed to identify the regulatory effects of miR-338-3p/phosphoinositide 3-kinase (PI3K)/Akt/thrombospondins 1 (THBS1) on glioma progression.
Materials and methods Quantitative reverse transcription polymerase chain reaction and western blotting were performed to evaluate the levels of miR-338-3p, THBS1, and PI3K/Akt phosphorylation-related proteins.TargetScan software predicted that miR-338-3p targeted THBS1.This was confirmed by performing the dual-luciferase assay.Wound-healing and cell-counting-kit-8 experiments were performed to analyze how THBS1 and miR-338-3p affect the ability of glioma cells to migrate and proliferate.
The effect of miR-338-3p on tumorigenicity in mice was also analyzed.Results miR-338-3p downregulation was observed in gliomas, whereas THBS1 showed the opposite trend.By suppressing the PI3K/Akt signaling pathway activation, miR-338-3p overregulated the ability of glioma cells to migrate and proliferate in vitro.Additionally, miR-338-3p inhibited the development of glioma tumors in vivo.
Moreover, miR-338-3p directly targeted THBS1.THBS1 overexpression promoted glioma cell migration and proliferation by Coaster increasing PI3K/Akt phosphorylation.Nonetheless, miR-338-3p overregulation alleviated the effects of THBS1 overexpression.Conclusion The miR-338-3p/PI3K/Akt/THBS1 regulatory axis can modulate the progression of glioma cell proliferation and migration; thus, it can be considered a therapeutic biomarker.