UBE2T-mediated HP1a ubiquitination enhances nucleolar function and promote the progression of IDH1/TP53-mutant glioma
This study provides critical insights into the role of UBE2T in IDH1/TP53 mutant glioma, a devastating disease with limited effective treatment options. We demonstrate that UBE2T, when overexpressed as a result of TP53 mutations, promotes glioma progression by enhancing nucleolar function and cell proliferation. The use of APR-246 to inhibit UBE2T presents a promising therapeutic strategy. This research not only advances our molecular understanding of glioma but also has direct translational implications, offering hope for more effective and personalized treatments for patients with this aggressive cancer.