白血病·淋巴瘤
白血病·淋巴瘤
백혈병·림파류
JOURNAL OF LEUKEMIA & LYMPHOMA
2013年
5期
263-266
,共4页
王丽娜%崔雪莹%马小彤%任倩%王楠
王麗娜%崔雪瑩%馬小彤%任倩%王楠
왕려나%최설형%마소동%임천%왕남
血液肿瘤%地西他滨%热休克蛋白22
血液腫瘤%地西他濱%熱休剋蛋白22
혈액종류%지서타빈%열휴극단백22
Hematologic neoplasms%Decitabine%Heat-shock protein 22
目的 探讨地两他滨(Aza-C)对造血系统肿瘤细胞热休克蛋白22(HSP22)表达的影响及可能的机制.方法 半定量反转录聚合酶链反应(PCR)法检测HSP22在造血系统肿瘤细胞系以及造血系统肿瘤患者骨髓单个核细胞中的表达水平;去甲基化药物Aza-C(2μmol/L)诱导上述细胞HSP22的表达;甲基化特异PCR法检测造血系统肿瘤细胞系、造血系统肿瘤患者和健康供者的骨髓单个核细胞中HSP22基因启动子甲基化状态.结果 在检测的13个造血系统肿瘤细胞系、20例不同类型的造血系统肿瘤患者以及10名健康供者骨髓单个核细胞中均未发现HSP22基因的表达;Aza-C能诱导造血系统肿瘤细胞系及造血系统肿瘤患者骨髓单个核细胞中的HSP22表达;Aza-C处理过的造血系统肿瘤细胞系中HSP22基因启动子处于部分去甲基化状态,健康供者及造血系统肿瘤患者骨髓单个核细胞HSP22基因启动子处于高甲基化状态.结论 Aza-C通过使HSP22基因启动子去甲基化诱导造血系统肿瘤细胞HSP22的表达.
目的 探討地兩他濱(Aza-C)對造血繫統腫瘤細胞熱休剋蛋白22(HSP22)錶達的影響及可能的機製.方法 半定量反轉錄聚閤酶鏈反應(PCR)法檢測HSP22在造血繫統腫瘤細胞繫以及造血繫統腫瘤患者骨髓單箇覈細胞中的錶達水平;去甲基化藥物Aza-C(2μmol/L)誘導上述細胞HSP22的錶達;甲基化特異PCR法檢測造血繫統腫瘤細胞繫、造血繫統腫瘤患者和健康供者的骨髓單箇覈細胞中HSP22基因啟動子甲基化狀態.結果 在檢測的13箇造血繫統腫瘤細胞繫、20例不同類型的造血繫統腫瘤患者以及10名健康供者骨髓單箇覈細胞中均未髮現HSP22基因的錶達;Aza-C能誘導造血繫統腫瘤細胞繫及造血繫統腫瘤患者骨髓單箇覈細胞中的HSP22錶達;Aza-C處理過的造血繫統腫瘤細胞繫中HSP22基因啟動子處于部分去甲基化狀態,健康供者及造血繫統腫瘤患者骨髓單箇覈細胞HSP22基因啟動子處于高甲基化狀態.結論 Aza-C通過使HSP22基因啟動子去甲基化誘導造血繫統腫瘤細胞HSP22的錶達.
목적 탐토지량타빈(Aza-C)대조혈계통종류세포열휴극단백22(HSP22)표체적영향급가능적궤제.방법 반정량반전록취합매련반응(PCR)법검측HSP22재조혈계통종류세포계이급조혈계통종류환자골수단개핵세포중적표체수평;거갑기화약물Aza-C(2μmol/L)유도상술세포HSP22적표체;갑기화특이PCR법검측조혈계통종류세포계、조혈계통종류환자화건강공자적골수단개핵세포중HSP22기인계동자갑기화상태.결과 재검측적13개조혈계통종류세포계、20례불동류형적조혈계통종류환자이급10명건강공자골수단개핵세포중균미발현HSP22기인적표체;Aza-C능유도조혈계통종류세포계급조혈계통종류환자골수단개핵세포중적HSP22표체;Aza-C처리과적조혈계통종류세포계중HSP22기인계동자처우부분거갑기화상태,건강공자급조혈계통종류환자골수단개핵세포HSP22기인계동자처우고갑기화상태.결론 Aza-C통과사HSP22기인계동자거갑기화유도조혈계통종류세포HSP22적표체.
Objective To investigate the effects and possible mechanisms of decitabine on heat-shock protein 22 (HSP22) expression in hematopoietic tumor cell lines and bone marrow samples from patients with hematopoietic tumor.Methods The expression of HSP22 in 13 hematopoietic tumor cell lines,20 primary patients' samples and 10 normal donor' samples were detected by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR).After HSP22 induction with a demethylating agent decitabine (2 μmol/L),the methylation of the HSP22 promoters in hematopoietic tumor cell lines,healthy donors and bone marrow samples from patients with hematopoietic tumor were detected by methylation specific PCR (MSP).Results Expression of HSP22 was not detected in 13 hematopoietic tumor cell lines,20 primary patients' samples or 10 healthy donors' samples.Decitabine can induce the expression of HSP22 in hematopoietic tumor cell lines and bone marrow samples from patients with hematopoietic tumor.Decitabine can maintain partially demethylation of HSP22 promoters in hematopoietic tumor cell lines.HSP22 promoters were highly methylated in BMMC of the healthy donors and patients with hcmatopoictic tumor.Conclusion Decitabine can induce the expression of HSP22 in hematopoietic tumor cells partly by demethylation of HSP22 promoters.