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RAD51B-AS1 通过上调 RAD51B 促进卵巢癌的恶性生物学行为。

RAD51B-AS1 promotes the malignant biological behavior of ovarian cancer through upregulation of RAD51B.

机构信息

Women's Reproductive Health Laboratory of Zhejiang Province, Women's Hospital, Zhejiang University School of Medicine, Hangzhou 310006, China.

Department of Gynecologic Oncology, Women's Hospital, Zhejiang University School of Medicine, Hangzhou 310006, China.

出版信息

J Zhejiang Univ Sci B. 2024 Jul 15;25(7):581-593. doi: 10.1631/jzus.B2300154.

DOI:10.1631/jzus.B2300154
PMID:39011678
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11254684/
Abstract

Long non-coding RNAs (lncRNAs) play an indispensable role in the occurrence and development of ovarian cancer (OC). However, the potential involvement of lncRNAs in the progression of OC is largely unknown. To investigate the detailed roles and mechanisms ofRAD51 homolog B-antisense 1 (), a novel lncRNA in OC, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to verify the expression of . Cellular proliferation, metastasis, and apoptosis were detected using the cell counting kit-8 (CCK-8), colony-formation, transwell, and flow cytometry assays. Mouse xenograft models were established for the detection of tumorigenesis. The results revealed that was significantly upregulated in a highly metastatic human OC cell line and OC tissues. significantly increased the proliferation and metastasis of OC cells and enhanced their resistance to anoikis. Biogenetics prediction analysis revealed that the only target gene of was . Subsequent gene function experiments revealed that exerts the same biological effects as . Rescue experiments demonstrated that the malignant biological behaviors promoted by overexpression were partially or completely reversed by silencing in vitro and in vivo. Thus, promotes the malignant biological behaviors of OC and activates the protein kinase B (Akt)/B cell lymphoma protein-2 (Bcl-2) signaling pathway, and these effects may be associated with the positive regulation of expression. is expected to serve as a novel molecular biomarker for the diagnosis and prediction of poor prognosis in OC, and as a potential therapeutic target for disease management.

摘要

长链非编码 RNA(lncRNA)在卵巢癌(OC)的发生和发展中起着不可或缺的作用。然而,lncRNA 参与 OC 进展的潜在机制在很大程度上尚不清楚。为了研究 RAD51 同源物 B-反义 1()作为 OC 中一种新的 lncRNA 的详细作用和机制,采用逆转录定量聚合酶链反应(RT-qPCR)验证的表达。使用细胞计数试剂盒-8(CCK-8)、集落形成、Transwell 和流式细胞术检测细胞增殖、转移和凋亡。建立小鼠异种移植模型以检测肿瘤发生。结果表明,在高度转移性人 OC 细胞系和 OC 组织中,显著上调。显著增加 OC 细胞的增殖和转移,并增强其对失巢凋亡的抵抗能力。生物遗传学预测分析显示,的唯一靶基因是。随后的基因功能实验表明,发挥与相同的生物学效应。挽救实验表明,体外和体内沉默可部分或完全逆转过表达促进的 OC 恶性生物学行为。因此,通过激活蛋白激酶 B(Akt)/B 细胞淋巴瘤蛋白-2(Bcl-2)信号通路,促进 OC 的恶性生物学行为,这些作用可能与的正调控表达有关。有望作为 OC 诊断和预后不良预测的新型分子生物标志物,以及疾病管理的潜在治疗靶点。

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