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Ubiquitin‐specific protease 22 ( USP 22) is a member of the “death‐from‐cancer” signature, which plays a key role in cancer progression. Previous evidence has shown that  USP 22 is overexpressed and correlates with poor prognosis in glioma. The effect and mechanism of  USP 22 in glioma malignancy, especially cancer stemness, remain elusive. Herein, we find  USP 22 is more enriched in stem‐like tumorspheres than differentiated glioma cells.  USP 22 knockdown inhibits cancer stemness in glioma cell lines. With a cell‐penetrating  TAT ‐tag protein, B cell‐specific Moloney murine leukemia virus integration site 1 ( BMI 1), a robust glioma stem‐cell marker, is found to mediate the effect of  USP 22 on glioma stemness. By immunofluorescence,  USP 22 and  BMI 1 are found to share similar intranuclear expression in glioma cells. By analysis with immunohistochemistry and bioinformatics,  USP 22 is found to positively correlate with  BMI 1 at the post‐translational level only rather than at the transcriptional level. By immunoprecipitation and in vivo deubiquitination assay,  USP 22 is found to interact with and deubiquitinate  BMI 1 for protein stabilization. Microarray analysis shows that  USP 22 and  BMI 1 mutually regulate a series of genes involved in glioma stemness such as   POSTN  ,   HEY 2 ,   PDGFRA   and   ATF 3 . In vivo study with nude mice confirms the role of  USP 22 in promoting glioma tumorigenesis by regulating  BMI 1. All these findings indicate  USP 22 as a novel deubiquitinase of  BMI 1 in glioma. We propose a working model of the  USP 22‐ BMI 1 axis, which promotes glioma stemness and tumorigenesis through oncogenic activation. Thus, targeting  USP 22 might be an effective strategy to treat glioma especially in those with elevated  BMI 1 expression.

cancer science

Ubiquitin‐specific protease 22 acts as an oncoprotein to maintain glioma malignancy through deubiquitinating B cell‐specific Moloney murine leukemia virus integration site 1 for stabilization