胃肠病学
胃腸病學
위장병학
CHINESE JOURNAL OF GASTROENTEROLOGY
2014年
5期
261-265
,共5页
陈微微%陈卫昌%岑建农%严苏
陳微微%陳衛昌%岑建農%嚴囌
진미미%진위창%잠건농%엄소
半乳糖凝集素3%胃肿瘤%RNA干扰%细胞增殖%细胞凋亡%化疗敏感性
半乳糖凝集素3%胃腫瘤%RNA榦擾%細胞增殖%細胞凋亡%化療敏感性
반유당응집소3%위종류%RNA간우%세포증식%세포조망%화료민감성
Galectin 3%Stomach Neoplasms%RNA Interference%Cell Proliferation%Apoptosis%Chemosensitivity
背景:Galectin-3属于半乳凝素家族成员,参与细胞生长和凋亡、细胞黏附、新生血管形成、肿瘤浸润和转移等多种生理和病理过程,在多种恶性肿瘤细胞中呈高表达。目的:研究 siRNA 干扰 galectin-3表达对人胃癌细胞株SGC-7901增殖、凋亡和化疗敏感性的影响。方法:合成靶向 galectin-3的 siRNA 并转染 SGC-7901细胞,以 real time PCR 和蛋白质印迹法检测干扰效果。CCK-8实验检测细胞增殖,流式细胞术检测细胞凋亡。结果:Galectin-3 siRNA 转染24 h 后转染效率为83.8%,转染后 SGC-7901细胞的 galectin-3表达显著受抑,mRNA 和蛋白表达量分别较空白对照组降低87.8%和90.4%(P <0.01)。转染后24 h、48 h 和72 h,galectin-3 siRNA 组 SGC-7901细胞增殖抑制率分别为15.57%±1.45%、32.90%±0.76%和57.35%±1.05%,转染后72 h 该组细胞凋亡率为46.17%±2.39%,均显著高于同时间点空白对照组、空脂质体组和阴性对照 siRNA 组(P <0.01)。Galectin-3 siRNA 组SGC-7901细胞由化疗药物奥沙利铂诱导的增殖抑制亦较其余三组显著增加(P <0.01)。结论:以 siRNA 干扰galectin-3表达后,SGC-7901细胞增殖减少、凋亡增加,对化疗药物的敏感性增强,表明 galectin-3有望成为胃癌基因治疗的有效靶点。
揹景:Galectin-3屬于半乳凝素傢族成員,參與細胞生長和凋亡、細胞黏附、新生血管形成、腫瘤浸潤和轉移等多種生理和病理過程,在多種噁性腫瘤細胞中呈高錶達。目的:研究 siRNA 榦擾 galectin-3錶達對人胃癌細胞株SGC-7901增殖、凋亡和化療敏感性的影響。方法:閤成靶嚮 galectin-3的 siRNA 併轉染 SGC-7901細胞,以 real time PCR 和蛋白質印跡法檢測榦擾效果。CCK-8實驗檢測細胞增殖,流式細胞術檢測細胞凋亡。結果:Galectin-3 siRNA 轉染24 h 後轉染效率為83.8%,轉染後 SGC-7901細胞的 galectin-3錶達顯著受抑,mRNA 和蛋白錶達量分彆較空白對照組降低87.8%和90.4%(P <0.01)。轉染後24 h、48 h 和72 h,galectin-3 siRNA 組 SGC-7901細胞增殖抑製率分彆為15.57%±1.45%、32.90%±0.76%和57.35%±1.05%,轉染後72 h 該組細胞凋亡率為46.17%±2.39%,均顯著高于同時間點空白對照組、空脂質體組和陰性對照 siRNA 組(P <0.01)。Galectin-3 siRNA 組SGC-7901細胞由化療藥物奧沙利鉑誘導的增殖抑製亦較其餘三組顯著增加(P <0.01)。結論:以 siRNA 榦擾galectin-3錶達後,SGC-7901細胞增殖減少、凋亡增加,對化療藥物的敏感性增彊,錶明 galectin-3有望成為胃癌基因治療的有效靶點。
배경:Galectin-3속우반유응소가족성원,삼여세포생장화조망、세포점부、신생혈관형성、종류침윤화전이등다충생리화병리과정,재다충악성종류세포중정고표체。목적:연구 siRNA 간우 galectin-3표체대인위암세포주SGC-7901증식、조망화화료민감성적영향。방법:합성파향 galectin-3적 siRNA 병전염 SGC-7901세포,이 real time PCR 화단백질인적법검측간우효과。CCK-8실험검측세포증식,류식세포술검측세포조망。결과:Galectin-3 siRNA 전염24 h 후전염효솔위83.8%,전염후 SGC-7901세포적 galectin-3표체현저수억,mRNA 화단백표체량분별교공백대조조강저87.8%화90.4%(P <0.01)。전염후24 h、48 h 화72 h,galectin-3 siRNA 조 SGC-7901세포증식억제솔분별위15.57%±1.45%、32.90%±0.76%화57.35%±1.05%,전염후72 h 해조세포조망솔위46.17%±2.39%,균현저고우동시간점공백대조조、공지질체조화음성대조 siRNA 조(P <0.01)。Galectin-3 siRNA 조SGC-7901세포유화료약물오사리박유도적증식억제역교기여삼조현저증가(P <0.01)。결론:이 siRNA 간우galectin-3표체후,SGC-7901세포증식감소、조망증가,대화료약물적민감성증강,표명 galectin-3유망성위위암기인치료적유효파점。
Background:Galectin-3 is a member of the galectin family that participates in a variety of physiological and pathological events including cell growth and apoptosis,cell adhesion,angiogenesis,as well as tumor invasion and metastasis,and has been reported to be overexpressed in many human cancers.Aims:To investigate the effect of galactin-3 targeted RNA interference on proliferation,apoptosis and chemosensitivity of human gastric cancer cell line SGC-7901. Methods:Galectin-3 targeted siRNA was constructed and transfected into SGC-7901 cells.Efficacy of RNA interference was evaluated by real time PCR and Western blotting,while cell proliferation was assessed by CCK-8 assay and cell apoptosis by flow cytometry.Results:The transfection efficiency at 24 hours after transfection was 83.8%;expression of galectin-3 in SGC-7901 cells was significantly inhibited at mRNA and protein levels with a decreasing of 87.8% and 90.4%,respectively (P <0.01).Proliferation inhibition rates of SGC-7901 cells in galectin-3 siRNA group at 24,48 and 72 hours after transfection were 15.57% ±1.45%,32.90% ±0.76% and 57.35% ±1.05%,respectively,and the apoptosis rate at 72 hours after transfection was 46.17% ±2.39%;all were significantly higher than those in blank control,liposome control and negative siRNA control groups at the same time points (P <0.01).Proliferation inhibition of SGC-7901 cells induced by oxaliplatin,a chemotherapeutic agent,was also markedly increased in galectin-3 siRNA group (P <0.01).Conclusions:Expression of galectin-3 in SGC-7901 cells can be inhibited successfully by RNA interference;cell proliferation is decreased,cell apoptosis is increased and sensitivity to chemotherapeutic agent is augmented,which indicates that galectin-3 is a promising target for gastric cancer gene therapy.