中南大学学报（医学版）
中南大學學報（醫學版）
중남대학학보（의학판）
JOURNAL OF CENTRAL SOUTH UNIVERSITY (MEDICAL SCIENCES)
2013年
12期
1217-1222
,共6页
黄军%李波%李坚%刘定阳%李岩%Walter A Hall%袁盾
黃軍%李波%李堅%劉定暘%李巖%Walter A Hall%袁盾
황군%리파%리견%류정양%리암%Walter A Hall%원순
非小细胞肺癌%脑转移瘤%免疫毒素%动物模型
非小細胞肺癌%腦轉移瘤%免疫毒素%動物模型
비소세포폐암%뇌전이류%면역독소%동물모형
non small cell lung cancer%metastatic brain tumor%immunotoxin%animal model
目的：观察免疫毒素DTATEGF对体外培养的人NSCLC脑转移瘤细胞增殖、凋亡及其对肿瘤血管生成的影响。方法：MTT法检测不同浓度靶向毒素DTATEGF对体外培养的人NSCLC脑转移瘤PC9-BrM3细胞增殖的影响，流式细胞仪分析DTATEGF作用于PC9-BrM3细胞系48 h后细胞凋亡和细胞周期变化。12只皮下种植肿瘤的祼小鼠分为2组：瘤床内分别注入DTATEGF或对照液2μg，隔天一次，共5次，测量肿瘤体积及其微血管密度(MVD)。结果：DTATEGF明显抑制PC9-BrM3细胞的体外增殖，呈剂量依赖关系，其诱导PC9-BrM3细胞凋亡，1 pmol/L的DTATEGF作用PC9-BrM3细胞48 h后细胞凋亡率为(64.0±0.5)%，对照组为(1.5±0.4)%，差异有统计学意义(P<0.01)；细胞周期检测显示：DTATEGF处理组SubG0/G1期和S期细胞别为(32.0±1.5)%和(2.0±0.4)%，而空白对照组分别为(5.0±0.6)%和(11.4±0.8)%，差异均有统计学意义(P<0.01)。动物实验显示DTATEGF处理组肿瘤体积较对照组生长缓慢，且DTATEGF处理组MVD为(15.6±4.6)/mm2，而空白对照组为(31.2±5.4)/mm2，差异均有统计学意义(P<0.05)。结论：DTATEGF抑制PC9-BrM3增殖、诱导细胞凋亡，明显抑制祼小鼠皮下种植的人NSCLC脑转移瘤细胞的生长及其新生血管的形成。
目的：觀察免疫毒素DTATEGF對體外培養的人NSCLC腦轉移瘤細胞增殖、凋亡及其對腫瘤血管生成的影響。方法：MTT法檢測不同濃度靶嚮毒素DTATEGF對體外培養的人NSCLC腦轉移瘤PC9-BrM3細胞增殖的影響，流式細胞儀分析DTATEGF作用于PC9-BrM3細胞繫48 h後細胞凋亡和細胞週期變化。12隻皮下種植腫瘤的祼小鼠分為2組：瘤床內分彆註入DTATEGF或對照液2μg，隔天一次，共5次，測量腫瘤體積及其微血管密度(MVD)。結果：DTATEGF明顯抑製PC9-BrM3細胞的體外增殖，呈劑量依賴關繫，其誘導PC9-BrM3細胞凋亡，1 pmol/L的DTATEGF作用PC9-BrM3細胞48 h後細胞凋亡率為(64.0±0.5)%，對照組為(1.5±0.4)%，差異有統計學意義(P<0.01)；細胞週期檢測顯示：DTATEGF處理組SubG0/G1期和S期細胞彆為(32.0±1.5)%和(2.0±0.4)%，而空白對照組分彆為(5.0±0.6)%和(11.4±0.8)%，差異均有統計學意義(P<0.01)。動物實驗顯示DTATEGF處理組腫瘤體積較對照組生長緩慢，且DTATEGF處理組MVD為(15.6±4.6)/mm2，而空白對照組為(31.2±5.4)/mm2，差異均有統計學意義(P<0.05)。結論：DTATEGF抑製PC9-BrM3增殖、誘導細胞凋亡，明顯抑製祼小鼠皮下種植的人NSCLC腦轉移瘤細胞的生長及其新生血管的形成。
목적：관찰면역독소DTATEGF대체외배양적인NSCLC뇌전이류세포증식、조망급기대종류혈관생성적영향。방법：MTT법검측불동농도파향독소DTATEGF대체외배양적인NSCLC뇌전이류PC9-BrM3세포증식적영향，류식세포의분석DTATEGF작용우PC9-BrM3세포계48 h후세포조망화세포주기변화。12지피하충식종류적관소서분위2조：류상내분별주입DTATEGF혹대조액2μg，격천일차，공5차，측량종류체적급기미혈관밀도(MVD)。결과：DTATEGF명현억제PC9-BrM3세포적체외증식，정제량의뢰관계，기유도PC9-BrM3세포조망，1 pmol/L적DTATEGF작용PC9-BrM3세포48 h후세포조망솔위(64.0±0.5)%，대조조위(1.5±0.4)%，차이유통계학의의(P<0.01)；세포주기검측현시：DTATEGF처리조SubG0/G1기화S기세포별위(32.0±1.5)%화(2.0±0.4)%，이공백대조조분별위(5.0±0.6)%화(11.4±0.8)%，차이균유통계학의의(P<0.01)。동물실험현시DTATEGF처리조종류체적교대조조생장완만，차DTATEGF처리조MVD위(15.6±4.6)/mm2，이공백대조조위(31.2±5.4)/mm2，차이균유통계학의의(P<0.05)。결론：DTATEGF억제PC9-BrM3증식、유도세포조망，명현억제관소서피하충식적인NSCLC뇌전이류세포적생장급기신생혈관적형성。
Objective:To investigate the in vitro and in vivo anticancer effcacy of the immunotoxin DTATEGF against human NSCLC brain metastatic tumor PC9-BrM3 cell line. <br> Methods:The effect of the immunotoxin DTATEGF was tested for its ability to inhibit the proliferation of PC9-BrM3 cells in vitro by MTT assay. The cell cycle and the apoptosis of cells with 1 pmol/L DTATEGF were examined by lfow cytometry. In vivo, 2μg of DTATEGF or control Bickel3 was given intratumor to nude mice with established PC9-BrM3 xenografts on their hips, andtumorvolumesweremeasuredandtumorsampleswereinvestigatedbyimmunchistochemistry SABC method. The microvessel density (MVD) was measured in each group. <br> Results:In vitro, DTATEGF killed PC9-BrM3 cells and showed an IC50 of 1 pmol/L. The apoptotic rate in the 1 pmol/L DTATEGF group was (64.0±0.5)%, signiifcantly higher than that in the control group (1.5±0.4)%(P<0.01). The cell cycle was obviously inhibited by DTATEGF in a dose-dependent manner. The percentage of cells treated with 1 pmol/L DTATEGF in SubG0/G1 phase was (32.0±1.5)%, significantly higher than that in the control group (2.0±0.4)%(P<0.01). In vivo, DTATEGF signiifcantly inhibited the growth of PC9-BrM3 hip tumors (P<0.05). The MVD of the DTATEGF group was (15.6±4.6)/mm2, signiifcantly lower than that of the control group (31.2±5.4)/mm2 (P<0.01). <br> Conclusion:DTATEGF inhibits the growth of the PC9-BrM3 cell line and induces its apoptosis. It is highly effcacious against human metastatic NSCLC brain tumor and against neovascularization.
