中国肿瘤临床
中國腫瘤臨床
중국종류림상
CHINESE JOURNAL OF CLINICAL ONCOLOGY
2013年
24期
1528-1530
,共3页
方念%方紫凌%张慧卿%韩小妮%黄根%王农荣%熊建萍%张焜和
方唸%方紫凌%張慧卿%韓小妮%黃根%王農榮%熊建萍%張焜和
방념%방자릉%장혜경%한소니%황근%왕농영%웅건평%장혼화
肝细胞癌%AFP%Survivin RNA干扰
肝細胞癌%AFP%Survivin RNA榦擾
간세포암%AFP%Survivin RNA간우
hepatocellular carcinoma%AFP%Survivin%RNA interference
目的:探讨肝癌HepG2细胞AFP基因沉默对Survivin表达的影响。方法:通过siRNA技术下调肝癌HepG2细胞中AFP的表达,采用ELISA法测定转染前后上清液AFP浓度,MTT法检测转染前后细胞增殖活性,流式细胞术分析细胞凋亡率, RT-PCR检测转染前后细胞Survivin mRNA水平。结果:转染48 h后,实验组上清液中AFP浓度显著下降,肝癌细胞生长活性下降43.1%,凋亡率增加24.3%,HepG2细胞中Survivin mRNA表达降低78.0%。对照组和空白组的上述指标均无明显变化。结论:沉默肝癌HepG2细胞AFP的表达,能有效抑制肝癌细胞生长、促进细胞凋亡,这一作用可能与细胞内Survivin mRNA水平降低有关。
目的:探討肝癌HepG2細胞AFP基因沉默對Survivin錶達的影響。方法:通過siRNA技術下調肝癌HepG2細胞中AFP的錶達,採用ELISA法測定轉染前後上清液AFP濃度,MTT法檢測轉染前後細胞增殖活性,流式細胞術分析細胞凋亡率, RT-PCR檢測轉染前後細胞Survivin mRNA水平。結果:轉染48 h後,實驗組上清液中AFP濃度顯著下降,肝癌細胞生長活性下降43.1%,凋亡率增加24.3%,HepG2細胞中Survivin mRNA錶達降低78.0%。對照組和空白組的上述指標均無明顯變化。結論:沉默肝癌HepG2細胞AFP的錶達,能有效抑製肝癌細胞生長、促進細胞凋亡,這一作用可能與細胞內Survivin mRNA水平降低有關。
목적:탐토간암HepG2세포AFP기인침묵대Survivin표체적영향。방법:통과siRNA기술하조간암HepG2세포중AFP적표체,채용ELISA법측정전염전후상청액AFP농도,MTT법검측전염전후세포증식활성,류식세포술분석세포조망솔, RT-PCR검측전염전후세포Survivin mRNA수평。결과:전염48 h후,실험조상청액중AFP농도현저하강,간암세포생장활성하강43.1%,조망솔증가24.3%,HepG2세포중Survivin mRNA표체강저78.0%。대조조화공백조적상술지표균무명현변화。결론:침묵간암HepG2세포AFP적표체,능유효억제간암세포생장、촉진세포조망,저일작용가능여세포내Survivin mRNA수평강저유관。
Objective:To observe the effects of AFP gene silencing by siRNA on the Survivin mRNA of hepatocellular carcino-ma cell line HepG2. Methods:AFP gene expression was downregulated in HepG2 cell by RNAi, and the AFP content in the superna-tant was detected by ELISA. Survivin mRNA level was tested by RT-PCR. MTT was applied to evaluate cell proliferation. Flow cytom-etry was employed to observe cell apoptosis. Results:At 48 h after transfection, AFP expression was almost completely inhibited, cell proliferation activity was decreased by 43.1%, cell apoptosis rate was increased by 24.3%, and the Survivin mRNA expression was re-duced to 22.0%in the experimental group. No evident changes were observed in negative control and blank groups. Conclusion:AFP gene silenced by RNAi induces growth inhibition and apoptosis promotion of hepatocellular carcinoma cell line HepG2. This gene may be associated with the suppression of Survivin mRNA.