原子核物理评论
原子覈物理評論
원자핵물리평론
Nuclear Physics Review
2015年
1期
110-114
,共5页
缪国英%张红%卢启明%李鸿岩%狄翠霞%郭逸潇
繆國英%張紅%盧啟明%李鴻巖%狄翠霞%郭逸瀟
무국영%장홍%로계명%리홍암%적취하%곽일소
细胞凋亡%重离子束%MSH2%基因表达
細胞凋亡%重離子束%MSH2%基因錶達
세포조망%중리자속%MSH2%기인표체
cell apoptosis%heavy ion beam%MSH2%gene expression
采用高传能线密度(LET)重离子辐照人胃癌SGC7901细胞,应用流式细胞技术、蛋白质印迹法(Western blot)及反转录聚合酶链式反应(RT-PCR)观察重离子诱导人胃癌SGC7901细胞周期、凋亡和MSH2表达状况。结果表明:与对照组相比, SGC7901细胞在辐射后72 h G2/M期所占细胞比率(33.26±0.08)和凋亡率(24.16±0.64)均达到峰值,且呈时间依赖性增加;经重离子照射后,DNA错配修复基因MSH2 mRNA和蛋白表达水平在6 h最高。结果提示:重离子在体外诱导SGC7901细胞周期阻滞和凋亡,且具有显著的时间依赖性效应;重离子在一定剂量和时间下,诱导了SGC7901细胞MSH2基因表达。DNA错配修复基因MSH2可能参与了重离子辐照诱导胃癌细胞DNA损伤的修复应答。
採用高傳能線密度(LET)重離子輻照人胃癌SGC7901細胞,應用流式細胞技術、蛋白質印跡法(Western blot)及反轉錄聚閤酶鏈式反應(RT-PCR)觀察重離子誘導人胃癌SGC7901細胞週期、凋亡和MSH2錶達狀況。結果錶明:與對照組相比, SGC7901細胞在輻射後72 h G2/M期所佔細胞比率(33.26±0.08)和凋亡率(24.16±0.64)均達到峰值,且呈時間依賴性增加;經重離子照射後,DNA錯配脩複基因MSH2 mRNA和蛋白錶達水平在6 h最高。結果提示:重離子在體外誘導SGC7901細胞週期阻滯和凋亡,且具有顯著的時間依賴性效應;重離子在一定劑量和時間下,誘導瞭SGC7901細胞MSH2基因錶達。DNA錯配脩複基因MSH2可能參與瞭重離子輻照誘導胃癌細胞DNA損傷的脩複應答。
채용고전능선밀도(LET)중리자복조인위암SGC7901세포,응용류식세포기술、단백질인적법(Western blot)급반전록취합매련식반응(RT-PCR)관찰중리자유도인위암SGC7901세포주기、조망화MSH2표체상황。결과표명:여대조조상비, SGC7901세포재복사후72 h G2/M기소점세포비솔(33.26±0.08)화조망솔(24.16±0.64)균체도봉치,차정시간의뢰성증가;경중리자조사후,DNA착배수복기인MSH2 mRNA화단백표체수평재6 h최고。결과제시:중리자재체외유도SGC7901세포주기조체화조망,차구유현저적시간의뢰성효응;중리자재일정제량화시간하,유도료SGC7901세포MSH2기인표체。DNA착배수복기인MSH2가능삼여료중리자복조유도위암세포DNA손상적수복응답。
Human gastric cancer cell SGC7901 were irradiated with high linear energy transfer (LET) carbon ion. Apoptotic cells after irradiation were analyzed by flow cytometry and expression of MSH2 genes in the irradiated cells was detected by western blot and RT-PCR assay. Compared with the control group, we found that the number of G2/M (33.26 ± 0.08) or apoptosis (24.16 ± 0.64) of SGC7901 cells reached a maximum after irradiation at 72 h in a dose dependent manner. And heavy ion irradiation e?ciently up-regulated the expression of MSH2 gene at 4.0 Gy after being irradiated 6 h. These results imply that heavy ion beam could induce cell apoptosis and cell cycle arrest in time-dependent manners. Furthermore, expression of MSH2 genes activated by carbon ion irradiation suggests that DNA mismatch repair gene MSH2 might be involved in DNA repair pathways.