Diagnostic, prognostic, and immune-related roles of G3BP1 in pan-cancer.

Abstract

Ras-GTPase-activating protein-binding protein 1 (G3BP1) is a core component and key regulatory switch of stress granules. It influences cell proliferation, differentiation, apoptosis, and RNA metabolism and is implicated in the pathogenesis of various diseases, including neurodegenerative disorders and myocardial hypertrophy, as well as in the regulation of innate immune responses. G3BP1 also plays a crucial role in the proliferation, invasion, and metastasis of cancer cells. However, a comprehensive pan-cancer analysis investigating its roles in diagnosis, prognosis, and immunological prediction has not yet been conducted. In this study, we integrated multiple databases to explore the potential carcinogenic functions of G3BP1. We analysed its expression patterns, prognostic relevance, immune cell infiltration, gene mutations, DNA methylation levels across various tumours, and functional states at the single-cell level and performed functional enrichment analysis of G3BP1-associated genes. Additionally, we examined G3BP1's interactions with chemicals and other genes. Our findings showed that G3BP1 is highly expressed in most cancers and is associated with poor patient prognosis. Moreover, G3BP1 demonstrated early diagnostic value in 10 tumour types and showed positive and negative correlations with prognosis depending on the tumour. Regarding tumour immunity, high G3BP1 expression was linked to an immunosuppressive tumour microenvironment and indicators of immunotherapy response. G3BP1 expression was negatively correlated with the infiltration of most immune cells but showed significant positive correlations with T helper cells and central memory T cells. Furthermore, we validated the overexpression of G3BP1 in cancer cells through in vitro experiments. Our study suggests that G3BP1 may serve as a diagnostic, prognostic, and immune-related biomarker in various cancers and could represent a potential target for tumour immunotherapy.