ArticleScientific reports2026
Identification of RBX1 as a regulator of LIPT1 transcription and its role in copper-induced cell death in GBM cells.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
This study aimed to investigate the expression and prognostic significance of genes associated with copper-induced cell death in glioblastoma multiforme (GBM). Using a suite of bioinformatics tools and databases, the researchers analyzed gene expression, survival rates, and immune infiltration in GBM. Complementary in vitro experiments were performed to evaluate the effects of LIPT1 inhibition on GBM cell behavior in the context of copper-induced cell death. The team further explored upstream mechanisms leading to LIPT1 overexpression in GBM, specifically focusing on transcription factors and the role of ubiquitination degradation. The findings indicated a significant upregulation of LIPT1 in GBM, correlating with increased sensitivity to copper-induced cell death. Inhibition of LIPT1 was observed to exacerbate malignant behaviors in GBM cells post-copper exposure. Subsequent analysis pinpointed three transcription factors—CBX3, E2F6, and GTF2B—as regulators of LIPT1. Notably, GTF2B was also found to be co-expressed with LIPT1 and positively associated with recurrence-free survival in patients. ChIP-seq data analysis revealed significant GTF2B binding peaks near the LIPT1 promoter. Further exploration using UbiBrowser 2.0 identified E3 ubiquitin ligases that potentially target GTF2B, with RBX1 emerging as a viable anti-cancer target in GBM. Data from the UALCAN database showed a notable decrease in RBX1 protein expression in GBM tissues. Moreover, several ubiquitination modification sites were detected on the GTF2B protein. In conclusion, the study proposes a novel scientific hypothesis: RBX1 inhibits LIPT1 transcription by promoting the ubiquitin-mediated degradation of GTF2B, thereby suppressing copper-induced cell death in GBM cells. These findings offer new insights into the molecular mechanisms governing copper death sensitivity in GBM and identify potential therapeutic targets for further exploration.
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