上皮性卵巢癌（EOC）是一种高发病率、快速转移且预后不佳的疾病。大多数女性在被诊断时处于中期或晚期，并具有较低的生存率。最近，长链非编码RNA（lncRNA）被认为在EOC发展中扮演关键角色。通过qPCR评估了SLC25A21反义RNA 1（SLC25A21-AS1）和多嘧啶轨迹结合蛋白3（PTBP3）在EOC细胞中的表达。通过EdU和Cell counting kit-8（CCK8）实验检测这些细胞的增殖活性，通过流式细胞术检测凋亡细胞的死亡率和细胞周期。通过Transwell实验检测细胞转移率。通过Western印迹法测量蛋白质表达。通过RNA免疫共沉淀（RIP）、IF-FISH共定位实验和电泳迁移率实验（EMSA）检测SLC25A21-AS1与PTBP3之间的相互作用。利用小鼠异种移植模型评估SLC25A21-AS1作为肿瘤抑制因子调节剂的重要性。与正常卵巢组织相比，lncRNA SLC25A21-AS1在卵巢癌组织中表达微不足道。一系列功能实验表明，SLC25A21-AS1的上调显著阻断了EOC细胞的增殖和转移，而其下调则产生相反的效果。在体内小鼠EOC模型中过表达SLC25A21-AS1导致肿瘤生长减缓和转移能力减弱。此外，SLC25A21-AS1降低了PTBP3的蛋白稳定性，并促进其降解。一系列随后的实验发现，通过泛素-蛋白酶体通路调节PTBP3，SLC25A21-AS1抑制EOC细胞的增殖和转移，而SLC25A21-AS1和PTBP3的组合则为功能实现提供了必要条件。我们的研究揭示了SLC25A21-AS1在EOC发展中的作用，并建议SLC25A21-AS1可以通过促进PTBP3的降解作为预后靶标以改善患者的生存率。©2023. The Author(s).

Epithelial ovarian cancer (EOC) is a highly prevalent disease that rapidly metastasizes and has poor prognosis. Most women are in the middle or late stages when diagnosed and have low survival rates. Recently, long non-coding RNAs (lncRNAs) were recognized to play pivotal roles in the development of EOC.The expression of SLC25A21 antisense RNA 1 (SLC25A21-AS1) and Polypyrimidine Tract Binding Protein 3 (PTBP3) in EOC cells was assessed via qPCR. The proliferation activity of these cells was detected by EdU and Cell counting kit-8 (CCK8) assays, while the death rate of apoptotic cells and the cell cycle were detected by flow cytometry. Detection of cell transfer rate by transwell assay. Protein expression was measured through western blotting. Interactions between SLC25A21-AS1 and PTBP3 were detected through RNA immunoprecipitation (RIP), IF-FISH co-localization experiments and electrophoretic mobility shift assay (EMSA). The in vivo importance of SLC25A21-AS1 as a tumor suppressor modulator was assessed using murine xenograft models.The lncRNA SLC25A21-AS1 has negligible expression in ovarian cancer tissues compared with that in normal ovarian tissues. A series of functional experiments revealed that the upregulation of SLC25A21-AS1 markedly blocked the proliferation and metastasis of EOC cells in vitro, while its downregulation had the opposite effect. Overexpression of SLC25A21-AS1 in a nude mouse model of EOC in vivo resulted in slower tumor growth and weakened metastatic potential. Moreover, SLC25A21-AS1 reduced the protein stability of PTBP3 and promoted its degradation. A series of subsequent experiments found that SLC25A21-AS1 inhibits EOC cell proliferation and metastasis by modulating PTBP3 through the ubiquitin-proteasome pathway and that the combination of SLC25A21-AS1 and PTBP3 provides the necessary conditions for the for the function to be realized.Our research reveals the effect of SLC25A21-AS1 in EOC development and suggests SLC25A21-AS1 can serve as a prognostic target by promoting the degradation of PTBP3 to improve patient survival.© 2023. The Author(s).