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作 者:韩崇旭[1] 许文荣[2] 王文兵[3] 孙艳[4] 乌慧玲[3]
机构地区:[1]苏北人民医院临床医学检测中心,江苏扬州225001 [2]江苏大学基础医学与医学技术学院,江苏镇江212013 [3]江苏大学生命科学研究院,江苏镇江212013 [4]苏北人民医院生殖医学中心,江苏扬州225001
出 处:《中华肿瘤防治杂志》2011年第23期1839-1842,共4页Chinese Journal of Cancer Prevention and Treatment
基 金:江苏省自然科学基金(BK2007072);江苏省卫生厅"科教兴卫工程"医学重点学科"实验诊断学"开放性课题(XK200723/WKF0809);江苏省苏北人民医院院内基金(yzuc-ms201039)
摘 要:目的:研究骨髓间质细胞(MSCs)诱导致瘤的发生机制。方法:采用荧光差异显示(FDD)技术寻找MSCs诱导致瘤(F6)的关键基因。将回收的差异关键基因片段,进行PCR再扩增,TA克隆cDNA片段,测序后经BLAST软件检索以进行同源性分析。结果:FDD成功分离了MSCs和F6肿瘤细胞之间的不同基因片段,TA克隆得到15个EST片段,GenBank序列比对分析表明,这些片断均与相关基因片断同源,其中C356、G392和G383分别与nu-cleostemin,CyclinⅠ和Siva基因同源,同源百分比分别为95%、97%和100%。结论:F6肿瘤细胞的发生机制是一个涉及到众多基因参与的复杂过程,nucleostemin、CyclinⅠ和Siva等基因在人类骨髓间质干细胞诱导突变转化为F6细胞的过程中起着重要作用。OBJECTIVE:To study of the molecular mechanism of human bone marrow mesenchymal stem cell(MSCs) induced into tumor cell(F6).METHODS:The associated key gene fragments were found to be used fluorescence label mRNA differential display technique between MSCs and F6 tumor cells were cut out from a polyacrylamide gel,re-amplified with the same primer pair.The inserts of clones were sequenced.Through BLAST software,the sequencing results were compared with GenBank database for homology analysis.RESULTS:Fifteen cDNA fragments were attained,and three of them(C356,G392 and G383) were highly up-regulated in F6 cells compared with MSCs.By comparing to the GeneBank databases,we found that C356,G392 and G383 fragments were 95%,97% and 100% homologous to nucleostemin,Cyclin Ⅰ and siva respectively.CONCLUSION:These findings support the idea that the increase of multiple genes including nucleostemin,Cyclin Ⅰ and siva expression in F6 may play a role in both tumorigenesis and transforming human bone marrow mesenchymal stem cells into F6 tumor cells.
关 键 词:骨髓细胞/细胞 间质干细胞 MRNA差异显示技术 肿瘤发生
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