Integrated analysis identifies myostatin as a potential biomarker and functional regulator in glioma

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Myostatin (MSTN), a member of the TGF-β superfamily, is recognized for its role in regulating muscle growth and cancer cachexia, but its involvement in glioma remains unclear. We examined MSTN expression and its clinical significance in glioma using public datasets and single-cell sequencing data. Immunohistochemistry and western blot further supported elevated MSTN protein levels in GBM tissues and cell lines. Knocking down MSTN in U87 and T98G cells revealed its impact on proliferation, migration, invasion, ROS accumulation, and apoptosis. Our analysis demonstrated that MSTN was significantly upregulated in glioma tissues and cell lines. Furthermore, ROC analysis indicated the diagnostic potential of MSTN in glioblastoma (GBM), lower-grade glioma (LGG), and the combined GBM-LGG cohort. High MSTN expression was associated with poorer survival in specific glioma subgroups, tumor heterogeneity, genomic instability-related features, and immune-related bioinformatic signatures. In vitro, siRNA-mediated MSTN depletion was associated with reduced glioblastoma cell proliferation, colony formation, migration, and invasion, together with increased ROS accumulation and apoptosis. Our findings suggest that MSTN upregulation in glioma could serve as a potential biomarker and might contribute to malignant phenotypes of glioma cells. Further studies are required to clarify the mechanistic role and clinical relevance of MSTN in glioma.

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