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

腫瘤基因檢測(cè)19800元導(dǎo)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(cè)LncRNA KCNQ1OT1揭示EIF2B5啟動(dòng)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(cè)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(jìn)了腫瘤的正確治療與個(gè)性化用藥的發(fā)展，進(jìn)一步強(qiáng)調(diào)了基因信息檢測(cè)與分析的重要性。

腫瘤靶向藥物及正確治療臨床研究?jī)?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(cè)臨床應(yīng)用結(jié)果

基因檢測(cè)阻止腫瘤轉(zhuǎn)移的項(xiàng)目背景：長(zhǎng)鏈非編碼 RNA (lncRNA) 在基因解碼結(jié)果中是人類(lèi)惡性腫瘤的調(diào)節(jié)因子，包括卵巢癌 (OC)。 LncRNA KCNQ1OT1 可以促進(jìn)卵巢癌進(jìn)展，而 EIF2B5 與幾種腫瘤的發(fā)展有關(guān)?；驒z測(cè)阻止腫瘤轉(zhuǎn)移的項(xiàng)目旨在探討lncRNA KCNQ1OT1在OC發(fā)育中的作用及其作用機(jī)制?；驒z測(cè)阻止腫瘤轉(zhuǎn)移的項(xiàng)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(cè)KCNQ1OT1和EIF2B5的基因表達(dá)水平。 通過(guò) MTT 和集落形成測(cè)定評(píng)估卵巢癌細(xì)胞增殖，并實(shí)施傷口愈合和 Transwell 測(cè)定以分別監(jiān)測(cè)細(xì)胞遷移和侵襲。通過(guò) MS-PCR基因檢測(cè)檢查 EIF2B5 啟動(dòng)子的甲基化狀態(tài)，以闡明 EIF2B5 的表達(dá)是否降低。 KCNQ1OT1 與甲基轉(zhuǎn)移酶 DNMT1、DNMT3A 和 DNMT3B 的結(jié)合活性通過(guò)雙熒光素酶報(bào)告基因測(cè)定或 RIP 測(cè)定來(lái)確定，以探索 KCNQ1OT1 改變其下游基因表達(dá)的潛力。 ChIP實(shí)驗(yàn)驗(yàn)證EIF2B5啟動(dòng)子與上述三種甲基轉(zhuǎn)移酶的結(jié)合?；驒z測(cè)阻止腫瘤轉(zhuǎn)移的項(xiàng)目結(jié)果：lncRNA KCNQ1OT1在OC組織和細(xì)胞中的表達(dá)增加。卵巢癌中 EIF2B5 表達(dá)下調(diào)，與 KCNQ1OT1 呈負(fù)相關(guān)。敲除 KCNQ1OT1 可抑制卵巢癌細(xì)胞增殖和轉(zhuǎn)移。 KCNQ1OT1 可以通過(guò)將 DNA 甲基轉(zhuǎn)移酶募集到 EIF2B5 啟動(dòng)子中來(lái)下調(diào) EIF2B5 的表達(dá)。此外，干擾 EIF2B5 表達(dá)挽救了 KCNQ1OT1 耗竭誘導(dǎo)的對(duì)卵巢癌細(xì)胞增殖和轉(zhuǎn)移的抑制作用?；驒z測(cè)阻止腫瘤轉(zhuǎn)移的項(xiàng)目結(jié)論：卵巢癌基因解碼基因檢測(cè)的研究結(jié)果證明 lncRNA KCNQ1OT1 通過(guò)降低 EIF2B5 表達(dá)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。基因檢測(cè)阻止卵巢癌轉(zhuǎn)移的項(xiàng)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(fù)轉(zhuǎn)移國(guó)際數(shù)據(jù)庫(kù)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.