PUF60 promotes glioblastoma progression through regulation of EGFR stability
Fang Wang1, Lan Peng1, Yikui Sun1
1The Affiliated Hospital of Medical School, Ningbo University, Ningbo, 315020, China.
Abstract:
PUF60 (Poly (U) binding splicing factor 60 kDa), a nucleic acid-binding protein, has been shown to regulate transcription and links to tumorigenesis in various cancers. However, its biological role and function in glioblastoma remain unknown. In this study, we found that PUF60 is highly expressed in glioblastoma and correlated with poor prognosis. Furthermore, PUF60 knockdown significantly decreased the proliferation of glioblastoma cells in vitro and in vivo. Mechanistically, PUF60 could reduce the ubiquitination level of EGFR by transcriptionally regulating STUB1, an E3 ubiquitin ligase of EGFR, which lead to the activation of the EGFR-AKT pathway. Collectively, our study reveals the oncogenic role of PUF60 in glioblastoma and provides a potential therapeutic target for glioblastoma treatment.
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