Expression of MCCC2 in glioma cells and preliminary verification of poor prognosis

This study mainly explored the regulatory role and mechanism of MCCC2 in GBM. This study verified the expression in clinical samples and GBM cell lines. CCK-8 and cell cloning experiments, flow cytometry, scratch experiments and Transwell chamber experiments were used to detect the effects of MCCC2 expression on proliferation, apoptosis, migration and invasion of GBM cells. A reduction in MCCC2 expression could significantly lower the protein levels of ERK, decrease p-ERK levels, and inhibit ERK phosphorylation. Ulixertinib, an ERK inhibitor, was shown to hinder the proliferation, migration, and invasion of GBM cells and counteract the regulatory impact of MCCC2 overexpression on GBM cells. This investigation revealed that suppressing MCCC2 expression impedes the proliferation, migration, and invasion of GBM cells and promotes GBM cell apoptosis by curtailing ERK expression and phosphorylation. This discovery implies that MCCC2 might serve as a potential biological target for anti-GBM therapy, laying the groundwork for future research in this field.