RNF122 promotes glioblastoma growth via the JAK2/STAT3/c-Myc signaling Axis

被引:1
作者
Xiao, Qingbao [1 ]
Xue, Kaming [2 ]
Li, Lin [3 ]
Zhu, Kai [3 ]
Fu, Rong [3 ]
Xiong, Zhiyong [3 ]
机构
[1] Wuhan Univ, Wuhan Hosp 3, Tongren Hosp, Dept Neurosurg, Wuhan, Hubei, Peoples R China
[2] Huazhong Univ Sci & Technol, Union Hosp, Dept Tradit Chinese Med, Tongji Med Coll, Wuhan, Hubei, Peoples R China
[3] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Neurosurg, 1277 Jiefang Ave, Wuhan 430022, Hubei, Peoples R China
关键词
glioblastoma; growth; JAK/STAT/c-Myc; RNF122; CANCER;
D O I
10.1111/cns.70017
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Objective The E3 ubiquitin ligase is well recognized as a significant contributor to glioblastoma (GBM) progression and has promise as a prospective therapeutic target. This study explores the contribution of E3 ubiquitin ligase RNF122 in the GBM progression and the related molecular mechanisms. Methods RNF122 expression levels were evaluated using qRT-PCR, WB, and IHC, while functional assays besides animal experiments were used to assess RNF122's effect on GBM progression. We also tested the RNF122 impact on JAK2/STAT3/c-Myc signaling using WB. ResultsRNF122 was upregulated in GBM and correlated to the advanced stage and poor clinical outcomes, representing an independent prognostic factor. Based on functional assays, RNF122 promotes GBM growth and cell cycle, which was validated further in subsequent analyses by JAK2/STAT3/c-Myc pathway activation. Moreover, JAK2/STAT3 signaling pathway inhibitor WP1066 can weaken the effect of overexpression RNF122 on promoting GBM progression. Conclusion Our results revealed that RNF122 caused an aggressive phenotype to GBM and was a poor prognosticator; thus, targeting RNF122 may be effectual in GBM treatment.
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页数:15
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