中国病理生理杂志
中國病理生理雜誌
중국병리생리잡지
CHINESE JOURNAL OF PATHOPHYSIOLOGY
2015年
5期
924-928
,共5页
吕心瑞%王保芳%王葆辉%徐晓%陈明亮
呂心瑞%王保芳%王葆輝%徐曉%陳明亮
려심서%왕보방%왕보휘%서효%진명량
MCPH1%电离辐射%MDC1%DNA双链损伤
MCPH1%電離輻射%MDC1%DNA雙鏈損傷
MCPH1%전리복사%MDC1%DNA쌍련손상
MCPH1%Irradiation%MDC1%DNA double-strand breaks
目的:研究MCPH1在电离辐射诱导食管癌细胞DNA损伤通路中的作用。方法:应用已构建的沉默MDC1的食管癌ECA109细胞株接受8 Gy电离辐射后1 h,检测相关因子核内斑点形成情况。构建沉默MCPH1的食管癌ECA109细胞株,检测此细胞株接受同样照射条件后相关因子核内斑点的形成情况。结果:成功构建沉默MCPH1的食管癌ECA109细胞;电离辐射使MDC1、MCPH1与γ-H2AX蛋白相互作用。沉默MDC1不影响γ-H2AX和MCPH1核内斑点的形成;沉默MCPH1使电离辐射导致的MDC1核内斑点减少,不影响γ-H2AX核内斑点的形成。结论:MCPH1在电离辐射诱导的DNA损伤通路中可能位于H2AX下游、MDC1上游,可以调控MDC1核内斑点形成。
目的:研究MCPH1在電離輻射誘導食管癌細胞DNA損傷通路中的作用。方法:應用已構建的沉默MDC1的食管癌ECA109細胞株接受8 Gy電離輻射後1 h,檢測相關因子覈內斑點形成情況。構建沉默MCPH1的食管癌ECA109細胞株,檢測此細胞株接受同樣照射條件後相關因子覈內斑點的形成情況。結果:成功構建沉默MCPH1的食管癌ECA109細胞;電離輻射使MDC1、MCPH1與γ-H2AX蛋白相互作用。沉默MDC1不影響γ-H2AX和MCPH1覈內斑點的形成;沉默MCPH1使電離輻射導緻的MDC1覈內斑點減少,不影響γ-H2AX覈內斑點的形成。結論:MCPH1在電離輻射誘導的DNA損傷通路中可能位于H2AX下遊、MDC1上遊,可以調控MDC1覈內斑點形成。
목적:연구MCPH1재전리복사유도식관암세포DNA손상통로중적작용。방법:응용이구건적침묵MDC1적식관암ECA109세포주접수8 Gy전리복사후1 h,검측상관인자핵내반점형성정황。구건침묵MCPH1적식관암ECA109세포주,검측차세포주접수동양조사조건후상관인자핵내반점적형성정황。결과:성공구건침묵MCPH1적식관암ECA109세포;전리복사사MDC1、MCPH1여γ-H2AX단백상호작용。침묵MDC1불영향γ-H2AX화MCPH1핵내반점적형성;침묵MCPH1사전리복사도치적MDC1핵내반점감소,불영향γ-H2AX핵내반점적형성。결론:MCPH1재전리복사유도적DNA손상통로중가능위우H2AX하유、MDC1상유,가이조공MDC1핵내반점형성。
AIM:To discover the effect of MCPH1 on the DNA damage induced by ionizing radiation in esoph-ageal cancer cells.METHODS:ECA109 cancer cells were radiated at dose of 8 Gy.The nuclear foci of relevant factors were detected 1 h after irradiation in the ECA109 cells after silence of MDC1 gene.A cell line was established that was sta-ble low expression of MCPH1.The nuclear foci induced by ionizing radiation after silence of MCPH1 were determined.RE-SULTS:The MCPH1 gene silenced ECA109 cell line was successfully constructed.A strong relationship between MDC1, MCPH1 andγ-H2AX was observed 1 h after 8 Gy irradiation.Silence of MDC1 did not affect the nuclear foci formation ofγ-H2AX and MCPH1.The nuclear foci of MDC1 but notγ-H2AX significantly reduced after silencing of MCPH1.CON-CLUSION:MCPH1 is located in the downstream of H2AX and upstream formation of MDC1, and regulates the nuclear fo-ci formation of MDC1 during DNA damage response.