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LncRNA INHEG promotes glioma stem cell maintenance and tumorigenicity through regulating rRNA 2’-O methylation

ABSTRACT: LncRNA INHEG promotes glioma stem cell maintenance and tumorigenicity through regulating rRNA 2’-O methylation

PROVIDER: PRJNA770523 | ENA |

REPOSITORIES: ENA

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LncRNA INHEG promotes glioma stem cell maintenance and tumorigenicity through regulating rRNA 2’-O methylation

Project description:Glioblastoma (GBM) ranks among the most lethal of human cancers, containing glioma stem cells (GSCs) that display therapeutic resistance. Here, we report that the lncRNA INHEG is highly expressed in GSCs compared to differentiated glioma cells (DGCs) and promotes GSC self-renewal through control of rRNA 2’-O-methylation. INHEG induces the interaction between a novel SUMO E3 ligase TAF15 and NOP58, a core component of snoRNP that guides rRNA methylation, to regulate NOP58 sumoylation and accelerate the C/D box snoRNP assembly. INHEG activation enhances rRNA 2’-O-methylation, thereby increasing the translation of oncogenic proteins including EGFR and IGF1R in glioma cells. Taken together, this study identifies a lncRNA that connects snoRNP-guided rRNA 2’-O-methylation to upregulated protein translation in GSCs, supporting a new axis for potential therapeutic targeting of gliomas.

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TGF-b-activated LncRNA LINC00115 is a critical regulator for glioma stem-like cell tumorigenicity

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