【佳学基因检测】基因检测LncRNA KCNQ1OT1揭示EIF2B5启动子甲基化引起卵巢癌转移和恶化

肿瘤基因检测19800元导读

根据肿瘤治疗的前沿研究知道《Mol Med》在. 2022 Sep 13;28(1):112.发表了一篇题目为《基因检测LncRNA KCNQ1OT1揭示EIF2B5启动子甲基化引起卵巢癌转移和恶化》肿瘤靶向药物治疗基因检测临床研究文章。该研究由Si-Li He, Ya-Ling Chen, Qi-Hua Chen, Qi Tian, Shui-Jing Yi 等完成。促进了肿瘤的正确治疗与个性化用药的发展，进一步强调了基因信息检测与分析的重要性。

肿瘤靶向药物及正确治疗临床研究内容关键词：

EIF2B5,入侵,转移,甲基化,卵巢癌,增殖, lncRNA KCNQ1OT1

肿瘤靶向治疗基因检测临床应用结果

基因检测阻止肿瘤转移的项目背景：长链非编码 RNA (lncRNA) 在基因解码结果中是人类恶性肿瘤的调节因子，包括卵巢癌 (OC)。 LncRNA KCNQ1OT1 可以促进卵巢癌进展，而 EIF2B5 与几种肿瘤的发展有关。基因检测阻止肿瘤转移的项目旨在探讨lncRNA KCNQ1OT1在OC发育中的作用及其作用机制。基因检测阻止肿瘤转移的项目方法：采用逆转录定量聚合酶链反应（RT-qPCR）或Western blotting检测KCNQ1OT1和EIF2B5的基因表达水平。 通过 MTT 和集落形成测定评估卵巢癌细胞增殖，并实施伤口愈合和 Transwell 测定以分别监测细胞迁移和侵袭。通过 MS-PCR基因检测检查 EIF2B5 启动子的甲基化状态，以阐明 EIF2B5 的表达是否降低。 KCNQ1OT1 与甲基转移酶 DNMT1、DNMT3A 和 DNMT3B 的结合活性通过双荧光素酶报告基因测定或 RIP 测定来确定，以探索 KCNQ1OT1 改变其下游基因表达的潜力。 ChIP实验验证EIF2B5启动子与上述三种甲基转移酶的结合。基因检测阻止肿瘤转移的项目结果：lncRNA KCNQ1OT1在OC组织和细胞中的表达增加。卵巢癌中 EIF2B5 表达下调，与 KCNQ1OT1 呈负相关。敲除 KCNQ1OT1 可抑制卵巢癌细胞增殖和转移。 KCNQ1OT1 可以通过将 DNA 甲基转移酶募集到 EIF2B5 启动子中来下调 EIF2B5 的表达。此外，干扰 EIF2B5 表达挽救了 KCNQ1OT1 耗竭诱导的对卵巢癌细胞增殖和转移的抑制作用。基因检测阻止肿瘤转移的项目结论：卵巢癌基因解码基因检测的研究结果证明 lncRNA KCNQ1OT1 通过降低 EIF2B5 表达水平加重卵巢癌转移，并为卵巢癌提供了一种新的治疗策略。基因检测阻止卵巢癌转移的项目关键词：EIF2B5 ;入侵；转移;甲基化；卵巢癌;增殖; lncRNA KCNQ1OT1。

肿瘤发生与反复转移国际数据库描述：

Background: Long non-coding RNAs (lncRNAs) have emerged as regulators of human malignancies, including ovarian cancer (OC). LncRNA KCNQ1OT1 could promote OC progression, and EIF2B5 was associated with development of several tumors. This project was aimed to explore the role of lncRNA KCNQ1OT1 in OC development, as well as the involving action mechanism.Methods: Reverse transcription quantitative polymerase chain reaction (RT-qPCR) or Western blotting was employed to determine the expression levels of KCNQ1OT1 and EIF2B5. OC cell proliferation was evaluated by MTT and colony formation assays, and wound healing and Transwell assays were implemented to monitor cell migration and invasion, respectively. The methylation status of EIF2B5 promoter was examined by MS-PCR, to clarify whether the expression of EIF2B5 was decreased. The binding activity of KCNQ1OT1 to methyltransferases DNMT1, DNMT3A and DNMT3B was determined by dual luciferase reporter assay or RIP assay, to explore the potential of KCNQ1OT1 alters the expression of its downstream gene. ChIP assay was carried out to verify the combination between EIF2B5 promoter and above three methyltransferases.Results: Expression of lncRNA KCNQ1OT1 was increased in OC tissues and cells. EIF2B5 expression was downregulated in OC, which was inversely correlated with KCNQ1OT1. Knockdown of KCNQ1OT1 inhibited OC cell proliferation and metastasis. KCNQ1OT1 could downregulate EIF2B5 expression by recruiting DNA methyltransferases into EIF2B5 promoter. Furthermore, interference of EIF2B5 expression rescued KCNQ1OT1 depletion-induced inhibitory impact on OC cell proliferation and metastasis.Conclusion: Our findings evidenced that lncRNA KCNQ1OT1 aggravated ovarian cancer metastasis by decreasing EIF2B5 expression level, and provided a novel therapeutic strategy for OC.Keywords: EIF2B5; Invasion; Metastasis; Methylation; Ovarian cancer; Proliferation; lncRNA KCNQ1OT1.