宁夏医科大学学报
寧夏醫科大學學報
저하의과대학학보
JOURNAL OF NINGXIA MEDICAL COLLEGE
2013年
8期
853-855,859
,共4页
王燕%王宁菊%丁静%廉斌%李少林
王燕%王寧菊%丁靜%廉斌%李少林
왕연%왕저국%정정%렴빈%리소림
乳腺癌%CacyBP/SIP基因%siRNA
乳腺癌%CacyBP/SIP基因%siRNA
유선암%CacyBP/SIP기인%siRNA
目的 探讨靶向钙周期素结合蛋白(CacyBP/SIP)基因的3对小干扰RNAs(small interference RNA,siRNAs)转染人乳腺癌细胞MDA-MB-231后,能否抑制CacyBP/SIP基因的表达.方法 化学合成3对CacyBP/SIP特异性siRNA(CacyBP/SIP-siRNA),分别转染MDA-MB-231细胞,RT-PCR法、Western blotting方法分别检测转染前后MDA-MB-231细胞的CacyBP/SIPmRNA和蛋白的水平.结果 CacyBP/SIP-siRNA001 成功转染入人乳腺癌MDA-MB-231细胞,RT-PCR结果显示,siRNA001组CacyBP/SIP mRNA的表达量为NC-siRNA阴性对照组的(25.2±1.34)%,siRNA002和siRNA003则为(64.8±0.58)%和(77.5±1.27)%,CacyBP/SIP-siRNA001 转染后能够抑制MDA-MB-231细胞中CacyBP/SIPmRNA,沉默效率为(74.8±0.75)% (P＜0.05),Western blotting证实了siRNA001的沉默作用.结论 CacyBP/SIP-siRNA001 能显著沉默MDA-MB-231 细胞中CacyBP/SIP mRNA和蛋白的表达.
目的 探討靶嚮鈣週期素結閤蛋白(CacyBP/SIP)基因的3對小榦擾RNAs(small interference RNA,siRNAs)轉染人乳腺癌細胞MDA-MB-231後,能否抑製CacyBP/SIP基因的錶達.方法 化學閤成3對CacyBP/SIP特異性siRNA(CacyBP/SIP-siRNA),分彆轉染MDA-MB-231細胞,RT-PCR法、Western blotting方法分彆檢測轉染前後MDA-MB-231細胞的CacyBP/SIPmRNA和蛋白的水平.結果 CacyBP/SIP-siRNA001 成功轉染入人乳腺癌MDA-MB-231細胞,RT-PCR結果顯示,siRNA001組CacyBP/SIP mRNA的錶達量為NC-siRNA陰性對照組的(25.2±1.34)%,siRNA002和siRNA003則為(64.8±0.58)%和(77.5±1.27)%,CacyBP/SIP-siRNA001 轉染後能夠抑製MDA-MB-231細胞中CacyBP/SIPmRNA,沉默效率為(74.8±0.75)% (P＜0.05),Western blotting證實瞭siRNA001的沉默作用.結論 CacyBP/SIP-siRNA001 能顯著沉默MDA-MB-231 細胞中CacyBP/SIP mRNA和蛋白的錶達.
목적 탐토파향개주기소결합단백(CacyBP/SIP)기인적3대소간우RNAs(small interference RNA,siRNAs)전염인유선암세포MDA-MB-231후,능부억제CacyBP/SIP기인적표체.방법 화학합성3대CacyBP/SIP특이성siRNA(CacyBP/SIP-siRNA),분별전염MDA-MB-231세포,RT-PCR법、Western blotting방법분별검측전염전후MDA-MB-231세포적CacyBP/SIPmRNA화단백적수평.결과 CacyBP/SIP-siRNA001 성공전염입인유선암MDA-MB-231세포,RT-PCR결과현시,siRNA001조CacyBP/SIP mRNA적표체량위NC-siRNA음성대조조적(25.2±1.34)%,siRNA002화siRNA003칙위(64.8±0.58)%화(77.5±1.27)%,CacyBP/SIP-siRNA001 전염후능구억제MDA-MB-231세포중CacyBP/SIPmRNA,침묵효솔위(74.8±0.75)% (P＜0.05),Western blotting증실료siRNA001적침묵작용.결론 CacyBP/SIP-siRNA001 능현저침묵MDA-MB-231 세포중CacyBP/SIP mRNA화단백적표체.
