RIT1 Promotes the Proliferation of Gliomas Through the Regulation of the PI3K/AKT/c-Myc Signalling Pathway

Abstract

Recently, RIT1 has been implicated in a range of neurological disorders; however, its precise function in glioma pathogenesis is not yet well-defined. This study employed quantitative reverse transcription PCR (qRT-PCR), Western blotting (WB), immunohistochemistry (IHC) and additional methodologies to assess RIT1 expression levels in glioma tissues. Furthermore, the study investigated its influence on glioma progression through a series of functional experiments. Animal models were also utilised to elucidate the mechanistic role of RIT1, with a particular focus on its effects on the PI3K/AKT signalling pathway. Research findings showcased that RIT1 is significantly overexpressed in gliomas and exhibits a strong correlation with tumour grade and unfavourable clinical outcomes. Furthermore, RIT1 serves as an independent prognostic marker of poor prognosis. Functional assays demonstrate that RIT1 facilitates the aggressiveness of glioma cells by activating the PI3K/AKT signalling. Additionally, it promotes tumour proliferation by inhibiting apoptosis and accelerating cell cycle progression. This study demonstrates that RIT1 significantly contributes to the aggressive phenotype and unfavourable prognosis of glioma, indicating its ability as a therapeutic target for glioma treatment.