中华神经外科杂志
中華神經外科雜誌
중화신경외과잡지
Chinese Journal of Neurosurgery
2011年
9期
964-968
,共5页
陈宏颉%王守森%郑兆聪%袁邦青%高进喜%刘峥%王如密%季天海
陳宏頡%王守森%鄭兆聰%袁邦青%高進喜%劉崢%王如密%季天海
진굉힐%왕수삼%정조총%원방청%고진희%류쟁%왕여밀%계천해
RNA干扰%STAT3转录因子%神经胶质瘤%肿瘤干细胞
RNA榦擾%STAT3轉錄因子%神經膠質瘤%腫瘤榦細胞
RNA간우%STAT3전록인자%신경효질류%종류간세포
RNA interference%STAT3 transcription factor%Glioma%Neoplastic stem cells
目的 建STAT3的RNAi载体干扰STAT3的表达,在体内外研究对胶质瘤干细胞的影响。方法 构建STAT3基因shRNA的腺病毒表达载体,感染人胶质瘤干细胞。采用RT -PCR、Western blot检测STAT3基因的干扰效果,用MTT和流式细胞仪检测干细胞的增殖、凋亡,并观察对荷瘤裸鼠的影响。结果转染重组腺病毒Ad - STAT3 siRNA后,胶质瘤干细胞的STAT3的mRNA表达率为(41.5±7.3)%,蛋白表达率为(31.2±6.4)%,细胞的增殖受到抑制,凋亡率为(23.8±6.1)%,同时荷瘤裸鼠的肿瘤生长受到抑制,生存期延长。结论重组腺病毒介导的STAT3 RNAi可显著抑制靶基因的表达与活化,显著抑制胶质瘤干细胞的生长功能,为基于胶质瘤干细胞的功能治疗提供了基础理论。
目的 建STAT3的RNAi載體榦擾STAT3的錶達,在體內外研究對膠質瘤榦細胞的影響。方法 構建STAT3基因shRNA的腺病毒錶達載體,感染人膠質瘤榦細胞。採用RT -PCR、Western blot檢測STAT3基因的榦擾效果,用MTT和流式細胞儀檢測榦細胞的增殖、凋亡,併觀察對荷瘤裸鼠的影響。結果轉染重組腺病毒Ad - STAT3 siRNA後,膠質瘤榦細胞的STAT3的mRNA錶達率為(41.5±7.3)%,蛋白錶達率為(31.2±6.4)%,細胞的增殖受到抑製,凋亡率為(23.8±6.1)%,同時荷瘤裸鼠的腫瘤生長受到抑製,生存期延長。結論重組腺病毒介導的STAT3 RNAi可顯著抑製靶基因的錶達與活化,顯著抑製膠質瘤榦細胞的生長功能,為基于膠質瘤榦細胞的功能治療提供瞭基礎理論。
목적 건STAT3적RNAi재체간우STAT3적표체,재체내외연구대효질류간세포적영향。방법 구건STAT3기인shRNA적선병독표체재체,감염인효질류간세포。채용RT -PCR、Western blot검측STAT3기인적간우효과,용MTT화류식세포의검측간세포적증식、조망,병관찰대하류라서적영향。결과전염중조선병독Ad - STAT3 siRNA후,효질류간세포적STAT3적mRNA표체솔위(41.5±7.3)%,단백표체솔위(31.2±6.4)%,세포적증식수도억제,조망솔위(23.8±6.1)%,동시하류라서적종류생장수도억제,생존기연장。결론중조선병독개도적STAT3 RNAi가현저억제파기인적표체여활화,현저억제효질류간세포적생장공능,위기우효질류간세포적공능치료제공료기출이론。
Objective To construct STAT3 siRNA to interfere the expression STAT3,and to observe the effect on glioblastoma stem cells. Method The adenovirus shRNA expression vector targeting STAT3 gene was constructed and transduced into glioblastoma stem cells. The gene silencing efficiency was monitored by RT - PCR and Western blot analysis. The proliferation and apoptosis of glioblastoma stem cells were detected by MTT assays and flow cytometry. In addition, the effect of tumor bearing mice was also observed. Results After the adenovirus STAT3 siRNA transfection, the level of mRNA decreased to (41.5 ±7.3)%, the level of protein decreased to( 31.2 ± 6. 4)%, the cell proliferation was inhibited, the cell apoptosis ratio increased to (23. 8 ± 6. 1 ) %. Additionly, the adenovirus STAT3 siRNA could inhibit the tumor growth and improve the lifespan of mice. Conclusions The adenovirus shRNA targeting STAT3 gene could significantly inhibit the expression and activation of STAT3, and suppress the proliferation of glioblastoma stem cells, which provide an ideal therapeutic strategy for treatment of glioblastoma stem cells.