【佳學基因檢測】基因檢測LncRNA KCNQ1OT1揭示EIF2B5啟動子甲基化引起卵巢癌轉(zhuǎn)移和惡化

腫瘤基因檢測19800元導讀

根據(jù)腫瘤治療的前沿研究知道《Mol Med》在.?2022 Sep 13;28(1):112.發(fā)表了一篇題目為《基因檢測LncRNA KCNQ1OT1揭示EIF2B5啟動子甲基化引起卵巢癌轉(zhuǎn)移和惡化》腫瘤靶向藥物治療基因檢測臨床研究文章。該研究由Si-Li He,?Ya-Ling Chen,?Qi-Hua Chen,?Qi Tian,?Shui-Jing Yi?等完成。促進了腫瘤的正確治療與個性化用藥的發(fā)展，進一步強調(diào)了基因信息檢測與分析的重要性。

腫瘤靶向藥物及正確治療臨床研究內(nèi)容關(guān)鍵詞：

EIF2B5,入侵,轉(zhuǎn)移,甲基化,卵巢癌,增殖, lncRNA KCNQ1OT1

腫瘤靶向治療基因檢測臨床應(yīng)用結(jié)果

基因檢測阻止腫瘤轉(zhuǎn)移的項目背景：長鏈非編碼 RNA (lncRNA) 在基因解碼結(jié)果中是人類惡性腫瘤的調(diào)節(jié)因子，包括卵巢癌 (OC)。 LncRNA KCNQ1OT1 可以促進卵巢癌進展，而 EIF2B5 與幾種腫瘤的發(fā)展有關(guān)?；驒z測阻止腫瘤轉(zhuǎn)移的項目旨在探討lncRNA KCNQ1OT1在OC發(fā)育中的作用及其作用機制?；驒z測阻止腫瘤轉(zhuǎn)移的項目方法：采用逆轉(zhuǎn)錄定量聚合酶鏈反應(yīng)（RT-qPCR）或Western blotting檢測KCNQ1OT1和EIF2B5的基因表達水平。 通過 MTT 和集落形成測定評估卵巢癌細胞增殖，并實施傷口愈合和 Transwell 測定以分別監(jiān)測細胞遷移和侵襲。通過 MS-PCR基因檢測檢查 EIF2B5 啟動子的甲基化狀態(tài)，以闡明 EIF2B5 的表達是否降低。 KCNQ1OT1 與甲基轉(zhuǎn)移酶 DNMT1、DNMT3A 和 DNMT3B 的結(jié)合活性通過雙熒光素酶報告基因測定或 RIP 測定來確定，以探索 KCNQ1OT1 改變其下游基因表達的潛力。 ChIP實驗驗證EIF2B5啟動子與上述三種甲基轉(zhuǎn)移酶的結(jié)合?；驒z測阻止腫瘤轉(zhuǎn)移的項目結(jié)果：lncRNA KCNQ1OT1在OC組織和細胞中的表達增加。卵巢癌中 EIF2B5 表達下調(diào)，與 KCNQ1OT1 呈負相關(guān)。敲除 KCNQ1OT1 可抑制卵巢癌細胞增殖和轉(zhuǎn)移。 KCNQ1OT1 可以通過將 DNA 甲基轉(zhuǎn)移酶募集到 EIF2B5 啟動子中來下調(diào) EIF2B5 的表達。此外，干擾 EIF2B5 表達挽救了 KCNQ1OT1 耗竭誘導的對卵巢癌細胞增殖和轉(zhuǎn)移的抑制作用?；驒z測阻止腫瘤轉(zhuǎn)移的項目結(jié)論：卵巢癌基因解碼基因檢測的研究結(jié)果證明 lncRNA KCNQ1OT1 通過降低 EIF2B5 表達水平加重卵巢癌轉(zhuǎn)移，并為卵巢癌提供了一種新的治療策略?；驒z測阻止卵巢癌轉(zhuǎn)移的項目關(guān)鍵詞：EIF2B5 ;入侵；轉(zhuǎn)移;甲基化；卵巢癌;增殖; lncRNA KCNQ1OT1。

腫瘤發(fā)生與反復轉(zhuǎn)移國際數(shù)據(jù)庫描述：

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.