中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2014年
11期
2417-2419
,共3页
梁寒晖%韦绵辉%张学荣%邓春红%蓝安科%蒙庆旭%宋武
樑寒暉%韋綿輝%張學榮%鄧春紅%藍安科%矇慶旭%宋武
량한휘%위면휘%장학영%산춘홍%람안과%몽경욱%송무
胃癌%贝伐单抗%血管内皮生长因子%白细胞介素-8%碱性成纤维细胞生长因子
胃癌%貝伐單抗%血管內皮生長因子%白細胞介素-8%堿性成纖維細胞生長因子
위암%패벌단항%혈관내피생장인자%백세포개소-8%감성성섬유세포생장인자
Gastric cancer%Bevacizumab%Vascular endothelial growth factor%Interleukin-8%Basic fibroblast growth factor
目的 对贝伐单抗治疗人类胃癌动物模型进行疗效分析,并筛选有效的生物标志物,为临床胃癌贝伐单抗的个性化治疗奠定基础.方法 建立3种胃移植癌裸鼠模型并给予贝伐单抗治疗,通过荧光原位杂交(FISH)分析人类表皮生长因子(HER2)基因表达,酶联免疫吸附试验(ELISA)和实时定量聚合酶链反应(Real-time PCR)分别检测血清中人血管内皮生长因子(VEGF)、白细胞介素8(IL-8)、碱性成纤维细胞生长因子(bFGF)和鼠VEGF的含量和mRNA的表达.结果 对照组裸鼠HER2基因表达存在明显扩增,而经贝伐单抗治疗4周后,3种肿瘤细胞模型组未见HER2基因扩增;肿瘤组织及血清中人VEGF、人IL-8、人bFGF及鼠VEGF的表达水平均显著降低,其中SGC-7901细胞株对照组中组织人VEGF为(316.7±134.7) pg/mg蛋白,治疗模型组为(99.1±52.6)pg/mg蛋白,对照组血清人VEGF为(44.8±5.7) ng/L,治疗模型组为(21.4±6.21) ng/L;且其相应mRNA表达水平也明显下降.结论 贝伐单抗可抑制小鼠胃癌的形成,并且在此过程中VEGF、IL-8和bFGF mRNA和蛋白表达水平的下降起重要作用.
目的 對貝伐單抗治療人類胃癌動物模型進行療效分析,併篩選有效的生物標誌物,為臨床胃癌貝伐單抗的箇性化治療奠定基礎.方法 建立3種胃移植癌裸鼠模型併給予貝伐單抗治療,通過熒光原位雜交(FISH)分析人類錶皮生長因子(HER2)基因錶達,酶聯免疫吸附試驗(ELISA)和實時定量聚閤酶鏈反應(Real-time PCR)分彆檢測血清中人血管內皮生長因子(VEGF)、白細胞介素8(IL-8)、堿性成纖維細胞生長因子(bFGF)和鼠VEGF的含量和mRNA的錶達.結果 對照組裸鼠HER2基因錶達存在明顯擴增,而經貝伐單抗治療4週後,3種腫瘤細胞模型組未見HER2基因擴增;腫瘤組織及血清中人VEGF、人IL-8、人bFGF及鼠VEGF的錶達水平均顯著降低,其中SGC-7901細胞株對照組中組織人VEGF為(316.7±134.7) pg/mg蛋白,治療模型組為(99.1±52.6)pg/mg蛋白,對照組血清人VEGF為(44.8±5.7) ng/L,治療模型組為(21.4±6.21) ng/L;且其相應mRNA錶達水平也明顯下降.結論 貝伐單抗可抑製小鼠胃癌的形成,併且在此過程中VEGF、IL-8和bFGF mRNA和蛋白錶達水平的下降起重要作用.
목적 대패벌단항치료인류위암동물모형진행료효분석,병사선유효적생물표지물,위림상위암패벌단항적개성화치료전정기출.방법 건립3충위이식암라서모형병급여패벌단항치료,통과형광원위잡교(FISH)분석인류표피생장인자(HER2)기인표체,매련면역흡부시험(ELISA)화실시정량취합매련반응(Real-time PCR)분별검측혈청중인혈관내피생장인자(VEGF)、백세포개소8(IL-8)、감성성섬유세포생장인자(bFGF)화서VEGF적함량화mRNA적표체.결과 대조조라서HER2기인표체존재명현확증,이경패벌단항치료4주후,3충종류세포모형조미견HER2기인확증;종류조직급혈청중인VEGF、인IL-8、인bFGF급서VEGF적표체수평균현저강저,기중SGC-7901세포주대조조중조직인VEGF위(316.7±134.7) pg/mg단백,치료모형조위(99.1±52.6)pg/mg단백,대조조혈청인VEGF위(44.8±5.7) ng/L,치료모형조위(21.4±6.21) ng/L;차기상응mRNA표체수평야명현하강.결론 패벌단항가억제소서위암적형성,병차재차과정중VEGF、IL-8화bFGF mRNA화단백표체수평적하강기중요작용.
Objective To analyze the efficacy of bevacizumab in the treatment of gastric cancer in mouse model,and screen effective biomarkers to evaluate the curative effect,laying a foundation for the personalized therapy for gastric cancer with bevacizumab.Methods Three gastric cancer animal models were established by transplanting three human/mouse gastric cancer cell lines into nude mice,and treated with bevacizumab.The curative effect was assessed by the size and weight of the tumors.Finally,the common biomarkers were detected:the expression of human epidermal growth factor receptor-2 (HER2) was examined by fluorescence in situ hybridization (FISH) ; enzyme linked immunosorbent assay (ELISA) and real-time quantitative polymerase chain reaction (Real-time PCR) were respectively employed to detect the protein and mRNA expression of human vascular endothelial growth factor (VEGF),interleukin (IL)-8,basic fibroblast growth factor (bFGF) and mouse VEGF.Results By FISH analysis,after treatment with bevacizumab for 4 weeks HER2 was undetectable in bevacizumab treated groups,but highly expressed in control group.Moreover,the mRNA and protein expression of human VEGF,IL-8,bFGF and mouse VEGF was reduced after treatment with bevacizumab.Specifically,in SGC-7901group after treatment with bevacizumab,the protein levels of human VEGF was decreased from (316.7 ± 134.7) pg/mg to (99.1 ± 52.6) pg/mg in tumor tissues,and those were declined from (44.8 ±5.7) ng/L to (21.4 ±6.21) ng/L in serum.Conclusion Bevacizumab can inhibit the formation of gastric tumor through down-regulating the mRNA and protein levels of VEGF,IL-8 and bFGF,suggesting that these three factors may act as important biomarkers in evaluating the clinical efficacy of bevacizumab in the treatment of gastric cancer.
