Dive into the groundbreaking research on how the SP140 inhibitor’s regulation of TRIM22 expression via the PI3K/AKT signaling pathway offers a promising avenue for glioma treatment advancements.
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SP140 inhibitor suppressing TRIM22 expression regulates glioma progress through PI3K/AKT signaling pathway.
Li et al., Brain Behav 2024
<!– DOI: 10.1002/brb3.3465 //–>
https://doi.org/10.1002/brb3.3465
The study delves into the role of the SP gene family, particularly SP100, SP110, SP140, and SP140L, in gliomas. Utilizing TCGA and CGGA datasets, it was found that SP family members are overexpressed in gliomas and negatively impact patient prognosis. Specifically, SP140 was identified as an independent prognostic factor. A predictive risk model/nomogram based on SP140 was developed and validated, showing high accuracy in forecasting glioma patient outcomes. The model’s effectiveness was confirmed through various analyses, including ROC curves and decision curve analyses.
Further investigation revealed that an SP140 inhibitor, GSK761, could inhibit glioma cell proliferation, migration, and invasion by downregulating TRIM22 expression and interfering with the PI3K/AKT signaling pathway. Additionally, SP140 and TRIM22 were found to coexpress in glioma cells, particularly those with high levels of vascular proliferation, and TRIM22 was linked to immune cell infiltration.
Significance: This research highlights the prognostic value of SP140 in gliomas and introduces a novel SP140-based nomogram for predicting patient survival. It also suggests a potential therapeutic target, where inhibiting SP140 could halt glioma progression through the TRIM22/PI3K/AKT pathway.