现代检验医学杂志
現代檢驗醫學雜誌
현대검험의학잡지
JOURNAL OF MODERN LABORATORY MEDICINE
2015年
2期
7-10
,共4页
慢性淋巴细胞白血病%miR-9-3%甲基化特异性聚合酶链反应%5-氮杂-2’-脱氧胞苷
慢性淋巴細胞白血病%miR-9-3%甲基化特異性聚閤酶鏈反應%5-氮雜-2’-脫氧胞苷
만성림파세포백혈병%miR-9-3%갑기화특이성취합매련반응%5-담잡-2’-탈양포감
CLL%miR-9-3%MSP%5-Aza2’Dc
目的：探讨 microRNA-9-3（miR-9-3）在慢性淋巴细胞白血病中的作用及调控机制。方法采用甲基化特异性聚合酶链反应（MSP）技术检测8例正常人骨髓组织和外周血、78例新确诊慢性淋巴细胞性白血病患者骨髓组织和7种白血病细胞系的甲基化水平；采用 Western blot 技术检测甲基化阳性白血病细胞株的 NF-κB1信号转导通路活化水平。结果正常对照组 miR-9-3启动子呈非甲基化状态；7种白血病细胞株中只有 I83-E95和 WAC3CD5＋两种细胞株种呈非甲基化状态（MSP 阳性率为28.6％）；78例慢性淋巴细胞性白血病患者中65例发生 miR-9-3甲基化（MSP 阳性率为83％）。去甲基化药物5-氮杂-2’-脱氧胞苷（5-Aza2’Dc）处理后的 I83-E95和 WAC3CD5＋细胞株 miR-9-3均处于去甲基化状态。结论慢性淋巴细胞性白血病患者存在 miR-9-3异常甲基化，可能导致癌细胞异常增生；miR-9-3去甲基化可抑制 NF-κB1信号通路活化，表明 miR-9-3可能可以通过该通路抑制癌细胞凋亡，引发患者疾病恶化；甲基化的白血病细胞株可被去甲基化药物抑制，因此 miR-9-3可以作为治疗慢性淋巴细胞白血病的新基因靶点。
目的：探討 microRNA-9-3（miR-9-3）在慢性淋巴細胞白血病中的作用及調控機製。方法採用甲基化特異性聚閤酶鏈反應（MSP）技術檢測8例正常人骨髓組織和外週血、78例新確診慢性淋巴細胞性白血病患者骨髓組織和7種白血病細胞繫的甲基化水平；採用 Western blot 技術檢測甲基化暘性白血病細胞株的 NF-κB1信號轉導通路活化水平。結果正常對照組 miR-9-3啟動子呈非甲基化狀態；7種白血病細胞株中隻有 I83-E95和 WAC3CD5＋兩種細胞株種呈非甲基化狀態（MSP 暘性率為28.6％）；78例慢性淋巴細胞性白血病患者中65例髮生 miR-9-3甲基化（MSP 暘性率為83％）。去甲基化藥物5-氮雜-2’-脫氧胞苷（5-Aza2’Dc）處理後的 I83-E95和 WAC3CD5＋細胞株 miR-9-3均處于去甲基化狀態。結論慢性淋巴細胞性白血病患者存在 miR-9-3異常甲基化，可能導緻癌細胞異常增生；miR-9-3去甲基化可抑製 NF-κB1信號通路活化，錶明 miR-9-3可能可以通過該通路抑製癌細胞凋亡，引髮患者疾病噁化；甲基化的白血病細胞株可被去甲基化藥物抑製，因此 miR-9-3可以作為治療慢性淋巴細胞白血病的新基因靶點。
목적：탐토 microRNA-9-3（miR-9-3）재만성림파세포백혈병중적작용급조공궤제。방법채용갑기화특이성취합매련반응（MSP）기술검측8례정상인골수조직화외주혈、78례신학진만성림파세포성백혈병환자골수조직화7충백혈병세포계적갑기화수평；채용 Western blot 기술검측갑기화양성백혈병세포주적 NF-κB1신호전도통로활화수평。결과정상대조조 miR-9-3계동자정비갑기화상태；7충백혈병세포주중지유 I83-E95화 WAC3CD5＋량충세포주충정비갑기화상태（MSP 양성솔위28.6％）；78례만성림파세포성백혈병환자중65례발생 miR-9-3갑기화（MSP 양성솔위83％）。거갑기화약물5-담잡-2’-탈양포감（5-Aza2’Dc）처리후적 I83-E95화 WAC3CD5＋세포주 miR-9-3균처우거갑기화상태。결론만성림파세포성백혈병환자존재 miR-9-3이상갑기화，가능도치암세포이상증생；miR-9-3거갑기화가억제 NF-κB1신호통로활화，표명 miR-9-3가능가이통과해통로억제암세포조망，인발환자질병악화；갑기화적백혈병세포주가피거갑기화약물억제，인차 miR-9-3가이작위치료만성림파세포백혈병적신기인파점。
Objective To investigate the role and regulatory mechanism of micro RNA-9-3 (miR-9-3)in the pathogenesis of chronic lymphocytic leukemia.Methods Using the methylation specific PCR (MSP)technology to detect 8 cases of normal bone marrow tissue and peripheral blood,78 cases of bone marrow tissue came from the chronic lymphocytic leukemia pateints newly diagnosed and the methylation level of 7 kinds of leukemia cell line.Used Western blot to detected the NF-kappa B1 signal transduction pathway activation levels of methylation positive leukemia cell line.Results The miR-9-3 of normal control group were in the negative methylation status.Only I83-E95 and WAC3CD5+ were in positive methylation status in seven kinds of leukemia cell line (the positive of MSP was 28.6%);65 cases occurred miR-9-3 methylated in 78 of chronic lymphocytic leukemia patients (the positive of MSP was 83%).I83-E95 and miR-9-3 cells of WAC3CD5+ were in the methylation state when treatment with 5-nitrogen-2’-deoxidization cytidine (5-Aza2’Dc).Conclusion The abnormal methylation of miR-9-3 were usually seenin chronic lymphocytic leukemia,it could lead to abnormal hyperplasis in cancer cells.The methylation of miR-9-3 could inhibit the activation of NF-kappa B1 signal pathway suggested that it could sup-press the apoptosis of cancer cells through this pathways to trogered the progression of disease.The inhibitor of methylation could be induced the demethylation of leukemia cell lines,so it is possible that miR-9-3 maight be a new gene targets for the treatment of chronic lymphocytic leukemia.
