中华普通外科杂志
中華普通外科雜誌
중화보통외과잡지
CHINESE JOURNAL OF GENERAL SURGERY
2011年
1期
45-47
,共3页
周保国%魏争%孙学溥%乔海泉
週保國%魏爭%孫學溥%喬海泉
주보국%위쟁%손학부%교해천
结肠肿瘤%基因表达%氟尿嘧啶%抗药性,肿瘤%RNA干扰
結腸腫瘤%基因錶達%氟尿嘧啶%抗藥性,腫瘤%RNA榦擾
결장종류%기인표체%불뇨밀정%항약성,종류%RNA간우
Colonic neoplasms%Gene expression%Fluorouracil%Drug resistance,neoplasm%RNA interference
目的 观察下调X连锁凋亡抑制蛋白(X-linked inhibitor of apoptosis protein,XIAP)基因表达后结肠癌细胞对5-氟尿嘧啶(5-Fu)敏感性的变化.方法 采用脂质体包裹方法将携带靶向干扰XIAP序列的表达载体转染人结肠癌细胞HCT-8和HCT116,观察结肠癌细胞生长活性的变化;应用5-Fu后,观察结肠癌细胞对5-Fu敏感性的变化,并应用蛋白印迹方法检测结肠癌细胞内凋亡相关因子caspase-3的活性变化. 结果抑制XIAP基因表达后,结肠癌细胞HCT-8和HCT116的生长活性受到有效抑制;结肠癌细胞HCT-8对5-Fu的耐药性得到逆转(P＜0.01),HCT116对5-Fu的敏感性得到明显提高(P＜0.05);结肠癌细胞内caspase-3的表达活性提高,5-Fu诱导细胞凋亡的活性得到增强. 结论XIAP的表达是结肠癌细胞HCT-8和HCT116对5-Fu耐药的一个重要机制;抑制XIAP基因表达后能够增强结肠癌细胞HCT-8和HCT116对5-Fu化疗的敏感性.
目的 觀察下調X連鎖凋亡抑製蛋白(X-linked inhibitor of apoptosis protein,XIAP)基因錶達後結腸癌細胞對5-氟尿嘧啶(5-Fu)敏感性的變化.方法 採用脂質體包裹方法將攜帶靶嚮榦擾XIAP序列的錶達載體轉染人結腸癌細胞HCT-8和HCT116,觀察結腸癌細胞生長活性的變化;應用5-Fu後,觀察結腸癌細胞對5-Fu敏感性的變化,併應用蛋白印跡方法檢測結腸癌細胞內凋亡相關因子caspase-3的活性變化. 結果抑製XIAP基因錶達後,結腸癌細胞HCT-8和HCT116的生長活性受到有效抑製;結腸癌細胞HCT-8對5-Fu的耐藥性得到逆轉(P＜0.01),HCT116對5-Fu的敏感性得到明顯提高(P＜0.05);結腸癌細胞內caspase-3的錶達活性提高,5-Fu誘導細胞凋亡的活性得到增彊. 結論XIAP的錶達是結腸癌細胞HCT-8和HCT116對5-Fu耐藥的一箇重要機製;抑製XIAP基因錶達後能夠增彊結腸癌細胞HCT-8和HCT116對5-Fu化療的敏感性.
목적 관찰하조X련쇄조망억제단백(X-linked inhibitor of apoptosis protein,XIAP)기인표체후결장암세포대5-불뇨밀정(5-Fu)민감성적변화.방법 채용지질체포과방법장휴대파향간우XIAP서렬적표체재체전염인결장암세포HCT-8화HCT116,관찰결장암세포생장활성적변화;응용5-Fu후,관찰결장암세포대5-Fu민감성적변화,병응용단백인적방법검측결장암세포내조망상관인자caspase-3적활성변화. 결과억제XIAP기인표체후,결장암세포HCT-8화HCT116적생장활성수도유효억제;결장암세포HCT-8대5-Fu적내약성득도역전(P＜0.01),HCT116대5-Fu적민감성득도명현제고(P＜0.05);결장암세포내caspase-3적표체활성제고,5-Fu유도세포조망적활성득도증강. 결론XIAP적표체시결장암세포HCT-8화HCT116대5-Fu내약적일개중요궤제;억제XIAP기인표체후능구증강결장암세포HCT-8화HCT116대5-Fu화료적민감성.
Objective To investigate sensitivity of colon cancer cells to 5-fluorouracil after downregulation of XIAP gene expression. Method Colon cancer cells HCT-8 and HCT116 were transfected with a short hairpin RNA targeted to XIAP by liposome, cells viability were examined.5-fluorouracil was applied into two kinds of colon cancer cells. Tumor cells sensitiviy to chemotherapeutic drug was evaluated. Caspase-3 activity in tumor cells was examined by Western blot. Result After downregulation of XIAP expression, cell growing viability of these two kinds of colon cancer cells was restricted, HCT-8 resistance to 5-fluorouracil was reversed ( P ＜ 0. 01 ), HCT116 sensitivity to 5-fluorouracil was enhanced (P ＜ 0.05), caspase-3 expression in colon cancer cells was highly activated, apoptosis inducing activity of 5-fluorouracil was increased significantly. Conclusions XIAP expression was a important mechanism in colon cancer cells HCT-8 and HCT 116 resistant to 5-fluorouracil, sensitivity to 5-fluorouracil of HCT-8 and HCT-116 was increased by downregulation of XIAP expression.
