CAJ | 학술논문

目的：探讨慢性粒细胞白血病细胞中影响miR-196b表达水平的表观遗传学因素。方法分别采用DNA甲基化转移酶抑制剂5-氮杂-2’-脱氧胞苷（5-Aza-2’-dc）、组蛋白去乙酰化酶抑制剂4-苯基丁酸（ PBA）和两者联合处理K562细胞，采用实时定量PCR（Real-time PCR）检测miR-196b的表达水平变化。结果 PBA的半数抑制浓度为1．58mmol/L。和正常人骨髓细胞miR-196b的表达水平相比，Aza组、PBA组和阴性对照组miR-196b的表达水平显著降低且基本一致，Aza＋PBA组miR-196b的表达水平和正常人表达水平基本一致。结论单独使用5-Aza-2’-dc或PBA不能使K562细胞中miR-196b的表达恢复正常，两者联合使用共同处理K562细胞，可使miR-196b的表达恢复正常，表明K562细胞中miR-196b的表达水平和基因组甲基化及组蛋白乙酰化均有关系。
목적：탐토만성립세포백혈병세포중영향miR-196b표체수평적표관유전학인소。방법분별채용DNA갑기화전이매억제제5-담잡-2’-탈양포감（5-Aza-2’-dc）、조단백거을선화매억제제4-분기정산（ PBA）화량자연합처리K562세포，채용실시정량PCR（Real-time PCR）검측miR-196b적표체수평변화。결과 PBA적반수억제농도위1．58mmol/L。화정상인골수세포miR-196b적표체수평상비，Aza조、PBA조화음성대조조miR-196b적표체수평현저강저차기본일치，Aza＋PBA조miR-196b적표체수평화정상인표체수평기본일치。결론단독사용5-Aza-2’-dc혹PBA불능사K562세포중miR-196b적표체회복정상，량자연합사용공동처리K562세포，가사miR-196b적표체회복정상，표명K562세포중miR-196b적표체수평화기인조갑기화급조단백을선화균유관계。
Objective To study if 5-Aza-2’-deoxycytidine along or together with 4-phenylbutyric acid could affect miR-196b expression levels in chronic myeloid leukemia cells .Methods K562 cells were treated with DNA methylation inhibitor 5-Aza-2’-deoxycytidine, histone deacetylase inhibitors 4-phenylbutyric acid separately and the combined treatment with both of them, then expression levels of miR-196b were detected using Real-time PCR.Results The half inhibition concentration of 4-phenylbutyric acid was 1.58mmol/L.Comparing with the expression level of miR-196b in normal human bone marrow cells, the expression levels of miR-196b were significantly lower in Aza group , PBA group and negative control cells and nearly consistent among three groups , and as high as normal cells in combined treatment group . Conclusion The expression level of miR-196b in K562 cells could not return to normal treated with 5-Aza-2 ’-deoxycytidine or 4-phenylbutyric acid separately , while could restore normal when treated with both agents , indicating that miR-196b expression level in K562 cells is related with both DNA methylation and histone acetylation .