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  • Title: RAD51B-AS1 promotes the malignant biological behavior of ovarian cancer through upregulation of RAD51B.
    Author: Wei X, Wang C, Tang S, Yang Q, Shen Z, Zhu J, Cheng X, Wang X, Xie X, Xu J, Lu W.
    Journal: J Zhejiang Univ Sci B; 2024 Jul 15; 25(7):581-593. PubMed ID: 39011678.
    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 (RAD51B-AS1), a novel lncRNA in OC, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to verify the expression of RAD51B-AS1. 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 RAD51B-AS1 was significantly upregulated in a highly metastatic human OC cell line and OC tissues. RAD51B-AS1 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 RAD51B-AS1 was RAD51B. Subsequent gene function experiments revealed that RAD51B exerts the same biological effects as RAD51B-AS1. Rescue experiments demonstrated that the malignant biological behaviors promoted by RAD51B-AS1 overexpression were partially or completely reversed by RAD51B silencing in vitro and in vivo. Thus, RAD51B-AS1 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 RAD51B expression. RAD51B-AS1 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. 长链非编码RNA（lncRNA）在卵巢癌的发生发展中起着不可或缺的作用，但它们在卵巢癌进展中的潜在作用在很大程度上仍是未知。为了研究新型lncRNA RAD51B-AS1在卵巢癌中的具体作用和机制，我们通过逆转录-定量聚合酶链反应实验验证了RAD51B-AS1的表达；使用CCK-8实验、集落形成实验、transwell实验和流式细胞术检测细胞的增殖、转移和凋亡水平；建立小鼠异种移植瘤模型检测肿瘤发生情况。结果显示：RAD51B-AS1在人高转移卵巢癌细胞系和卵巢癌组织中显著上调；同时，RAD51B-AS1显著增强卵巢癌细胞的增殖、转移和抵抗失巢凋亡的能力。生物遗传学预测分析显示，RAD51B-AS1的唯一靶基因为RAD51B。随后的基因功能实验表明，RAD51B与RAD51B-AS1具有相同的生物学效应。体外和体内实验均表明，过表达RAD51B-AS1促进的恶性生物学行为可以通过沉默RAD51B的表达部分或完全逆转。由此可见，RAD51B-AS1可促进卵巢癌的恶性生物学行为，并激活Akt/Bcl-2信号通路，这些作用可能与其正向调节RAD51B的表达有关。RAD51B-AS1有望作为一种新的分子生物标志物，用于卵巢癌不良预后的诊断和预测，并作为疾病管理的潜在治疗靶点。. 长链非编码RNA（lncRNA）在卵巢癌的发生发展中起着不可或缺的作用，但它们在卵巢癌进展中的潜在作用在很大程度上仍是未知。为了研究新型lncRNA RAD51B-AS1在卵巢癌中的具体作用和机制，我们通过逆转录-定量聚合酶链反应实验验证了RAD51B-AS1的表达；使用CCK-8实验、集落形成实验、transwell实验和流式细胞术检测细胞的增殖、转移和凋亡水平；建立小鼠异种移植瘤模型检测肿瘤发生情况。结果显示：RAD51B-AS1在人高转移卵巢癌细胞系和卵巢癌组织中显著上调；同时，RAD51B-AS1显著增强卵巢癌细胞的增殖、转移和抵抗失巢凋亡的能力。生物遗传学预测分析显示，RAD51B-AS1的唯一靶基因为RAD51B。随后的基因功能实验表明，RAD51B与RAD51B-AS1具有相同的生物学效应。体外和体内实验均表明，过表达RAD51B-AS1促进的恶性生物学行为可以通过沉默RAD51B的表达部分或完全逆转。由此可见，RAD51B-AS1可促进卵巢癌的恶性生物学行为，并激活Akt/Bcl-2信号通路，这些作用可能与其正向调节RAD51B的表达有关。RAD51B-AS1有望作为一种新的分子生物标志物，用于卵巢癌不良预后的诊断和预测，并作为疾病管理的潜在治疗靶点。
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