PRC1 promotes ovarian cancer progression by binding to RPL4 and increasing MDM2-mediated p53 ubiquitination

IF 3.5 3区 生物学 Q3 CELL BIOLOGY Experimental cell research Pub Date : 2025-04-15 Epub Date: 2025-03-13 DOI:10.1016/j.yexcr.2025.114509
Yinyin Xu , Jiaxing Xu , Kai Xu , Cancan Zhang , Fengmian Wang , Rong Zhang , Pengfeng Zhu
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Abstract

Ovarian cancer (OC) is one of the most fatal gynecological carcinomas, causing significant detriment to women's health. Protein regulator of cytokinesis 1 (PRC1) is a microtubule-associated protein that is found to be highly expressed in many different cancers. Despite this, the exact way in which PRC1 stimulates the growth of OC has yet to be completely understood. Our research demonstrated that PRC1 expression was increased in OC, which was closely related to poor prognosis. Moreover, PRC1 exhibited noteworthy efficacy in enhancing the proliferation and migration capacities of OC cells, as well as affecting the cell cycle in OC cells. Silencing PRC1 significantly suppressed OC growth in vivo. Mechanically, PRC1 could interact with RPL4, which caused a decrease in RPL4/MDM2 complex formation, resulting in the enhanced ubiquitination of p53 and a reduction of p53 proteins. These findings revealed that PRC1 was involved in the RPL4-MDM2-p53 pathway thus playing a tumorigenic role on OC.
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PRC1通过结合RPL4和增加mdm2介导的p53泛素化来促进卵巢癌的进展。
卵巢癌(OC)是最致命的妇科肿瘤之一,严重危害妇女健康。细胞分裂1蛋白调节因子(PRC1)是一种微管相关蛋白,在许多不同的癌症中被发现高表达。尽管如此,PRC1刺激OC生长的确切方式尚不完全清楚。我们的研究表明,在OC中PRC1表达升高,与预后不良密切相关。此外,PRC1在增强OC细胞的增殖和迁移能力以及影响OC细胞周期方面表现出显著的功效。沉默PRC1可显著抑制OC在体内的生长。机械上,PRC1可以与RPL4相互作用,导致RPL4/MDM2复合物形成减少,导致p53泛素化增强,p53蛋白减少。这些发现表明PRC1参与RPL4-MDM2-p53通路,从而在OC中起致瘤作用。
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来源期刊
Experimental cell research
Experimental cell research 医学-细胞生物学
CiteScore
7.20
自引率
0.00%
发文量
295
审稿时长
30 days
期刊介绍: Our scope includes but is not limited to areas such as: Chromosome biology; Chromatin and epigenetics; DNA repair; Gene regulation; Nuclear import-export; RNA processing; Non-coding RNAs; Organelle biology; The cytoskeleton; Intracellular trafficking; Cell-cell and cell-matrix interactions; Cell motility and migration; Cell proliferation; Cellular differentiation; Signal transduction; Programmed cell death.
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