详细信息

RRP9 promotes prostate cancer metastasis and epithelial-mesenchymal transition through activation of the AKT/GSK3β/β-Catenin signaling pathway  ( SCI-EXPANDED收录)  

文献类型:期刊文献

英文题名:RRP9 promotes prostate cancer metastasis and epithelial-mesenchymal transition through activation of the AKT/GSK3β/β-Catenin signaling pathway

作者:Da, Zijian[1];Du, Yadan[2];Chen, Yawen[2];Da, Mingxu[1,3];Zhou, Fenghai[1,4]

第一作者:Da, Zijian

通信作者:Zhou, FH[1];Zhou, FH[2]

机构:[1]Lanzhou Univ, Sch Clin Med 1, Lanzhou 730000, Peoples R China;[2]Gansu Univ Tradit Chinese Med, Clin Coll 1, Lanzhou 730000, Peoples R China;[3]Gansu Prov Hosp, Dept Surg Oncol, Lanzhou 730000, Peoples R China;[4]Gansu Prov Hosp, Dept Urol, Lanzhou 730000, Peoples R China

第一机构:Lanzhou Univ, Sch Clin Med 1, Lanzhou 730000, Peoples R China

通信机构:[1]corresponding author), Lanzhou Univ, Sch Clin Med 1, Lanzhou 730000, Peoples R China;[2]corresponding author), Gansu Prov Hosp, Dept Urol, Lanzhou 730000, Peoples R China.

年份:2025

卷号:16

期号:1

外文期刊名:DISCOVER ONCOLOGY

收录:;Scopus(收录号:2-s2.0-105008248332);WOS:【SCI-EXPANDED(收录号:WOS:001510581300003)】;

基金:This research was supported by the Gansu Provincial Hospital (Grant number: 22GSSYD-16) and the First Hospital of Lanzhou University (Grant number: Ldyyyn2023-33).

语种:英文

外文关键词:RRP9; AKT; GSK3 beta; beta-catenin; Prostate cancer; Metastasis; Epithelial-mesenchymal transition

摘要:Ribosomal RNA Processing 9 (RRP9) is a gene associated with ribosomal function, and studies have demonstrated that its expression is aberrantly regulated in various tumor types, correlating with tumor progression. However, the specific role and underlying mechanism of RRP9 in prostate cancer (PCa) remain largely unexplored. In this study, bioinformatics analysis revealed that RRP9 is upregulated in PCa and is significantly associated with poor prognosis and lymph node metastasis. Further experimental data demonstrated that RRP9 knockdown notably inhibited the metastasis, invasion, and epithelial-mesenchymal transition (EMT) of PCa. Conversely, overexpression of RRP9 activated the AKT signaling pathway, resulting in the phosphorylation of GSK3 beta at Ser9, which in turn prevented beta-catenin degradation and promoted cell metastasis, invasion, and EMT. Rescue experiments demonstrated that SC79 effectively reversed the inhibitory effects of RRP9 knockdown on PCa. These findings highlight the potential role of RRP9 in promoting the malignant biological behaviors of PCa, providing new insights and potential therapeutic strategies for the treatment of the disease.

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