中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2014年
2期
236-238
,共3页
杨锐%王桂华%李小兰%邹声泉%胡俊波
楊銳%王桂華%李小蘭%鄒聲泉%鬍俊波
양예%왕계화%리소란%추성천%호준파
p55PIK%血管内皮生长因子%血管生成%结肠肿瘤
p55PIK%血管內皮生長因子%血管生成%結腸腫瘤
p55PIK%혈관내피생장인자%혈관생성%결장종류
p55PIK%Vascular endothelial growth factor%Angiogenesis%Colon cancer
目的 观察p55PIK对结肠癌细胞(HT29)的血管内皮生长因子(VEGF)分泌及其对成瘤的影响,探讨肿瘤中p55PIK与血管生成之间的关系.方法 以携带有p55PIK基因的腺病毒感染肿瘤细胞,用实时定量聚合酶链反应(Real-time PCR)检测空白组以及感染空腺病毒和p55PIK腺病毒的肿瘤细胞中VEGF mRNA水平表达差异;用Western blot的方法检测肿瘤细胞VEGF蛋白水平的表达差异;并以感染空腺病毒和感染p55PIK腺病毒的HT29细胞种植裸鼠,观察p55PIK对成瘤性的影响;以移植瘤行免疫组织化学染色,比较p55PIK、VEGF和CD31在组织中表达水平的差异.结果 细胞内过表达p55PIK后,VEGF mRNA表达水平较对照组和空腺病毒组增高2.7倍(P＜0.01),蛋白表达水平也明显增高(P＜0.01);成瘤性明显增强,移植瘤的生长速度增快,3组肿瘤重量分别为(0.057 ±0.040)、(0.060±0.030)、(0.225 ±0.070) g(P ＜0.01).过表达p55PIK组的肿瘤组织中VEGF和CD31的表达水平明显增高.结论 过表达p55PIK的肿瘤细胞成瘤性的增强可能是通过提高VEGF的表达,从而促进肿瘤血管的生成来实现的.
目的 觀察p55PIK對結腸癌細胞(HT29)的血管內皮生長因子(VEGF)分泌及其對成瘤的影響,探討腫瘤中p55PIK與血管生成之間的關繫.方法 以攜帶有p55PIK基因的腺病毒感染腫瘤細胞,用實時定量聚閤酶鏈反應(Real-time PCR)檢測空白組以及感染空腺病毒和p55PIK腺病毒的腫瘤細胞中VEGF mRNA水平錶達差異;用Western blot的方法檢測腫瘤細胞VEGF蛋白水平的錶達差異;併以感染空腺病毒和感染p55PIK腺病毒的HT29細胞種植裸鼠,觀察p55PIK對成瘤性的影響;以移植瘤行免疫組織化學染色,比較p55PIK、VEGF和CD31在組織中錶達水平的差異.結果 細胞內過錶達p55PIK後,VEGF mRNA錶達水平較對照組和空腺病毒組增高2.7倍(P＜0.01),蛋白錶達水平也明顯增高(P＜0.01);成瘤性明顯增彊,移植瘤的生長速度增快,3組腫瘤重量分彆為(0.057 ±0.040)、(0.060±0.030)、(0.225 ±0.070) g(P ＜0.01).過錶達p55PIK組的腫瘤組織中VEGF和CD31的錶達水平明顯增高.結論 過錶達p55PIK的腫瘤細胞成瘤性的增彊可能是通過提高VEGF的錶達,從而促進腫瘤血管的生成來實現的.
목적 관찰p55PIK대결장암세포(HT29)적혈관내피생장인자(VEGF)분비급기대성류적영향,탐토종류중p55PIK여혈관생성지간적관계.방법 이휴대유p55PIK기인적선병독감염종류세포,용실시정량취합매련반응(Real-time PCR)검측공백조이급감염공선병독화p55PIK선병독적종류세포중VEGF mRNA수평표체차이;용Western blot적방법검측종류세포VEGF단백수평적표체차이;병이감염공선병독화감염p55PIK선병독적HT29세포충식라서,관찰p55PIK대성류성적영향;이이식류행면역조직화학염색,비교p55PIK、VEGF화CD31재조직중표체수평적차이.결과 세포내과표체p55PIK후,VEGF mRNA표체수평교대조조화공선병독조증고2.7배(P＜0.01),단백표체수평야명현증고(P＜0.01);성류성명현증강,이식류적생장속도증쾌,3조종류중량분별위(0.057 ±0.040)、(0.060±0.030)、(0.225 ±0.070) g(P ＜0.01).과표체p55PIK조적종류조직중VEGF화CD31적표체수평명현증고.결론 과표체p55PIK적종류세포성류성적증강가능시통과제고VEGF적표체,종이촉진종류혈관적생성래실현적.
Objective To study the effect of p55PIK on colon tumor cells (HT29) secreting vascular endothelial growth factor (VEGF) and tumorgenesis,and the relationship between p55PIK and angiogenesis in tumors.Methods The tumor cells were infected by adenovirus coding p55PIK-GFP,and the mRNA and protein expression level of VEGF in blank control group,empty vector group and p55PIK vector group was detected by using real-time quantitative polymerase chain reaction (Real-time PCR) and Western blotting respectively.In animal study,nude mice xenograft model was made by injecting HT29 cells infected by adenovirus carrying control vector or p55PIK vector respectively.The effect of p55PIK on tumorgenesis was observed,and the expression of p55PIK,VEGF and CD31 in the xenograft of mice was detected by using immunohistochemitry.Results The mRNA level of VEGF in p55PIK vector group was 2.7 times higher in blank control group and empty control group,so was the protein level (P ＜ 0.01).Meanwhile,the tumorigenic ability and growth speed of the xenograft were increased.The average tumor weight in blank control group,empty vector group and p55 PIK vector group was (0.057 ± 0.040) g,(0.060 ±0.030) g and (0.225 ±0.070) g respectively (P ＜0.01).The expression of VEGF and CD31 in xenograft of mice was significantly increased in p55PIK-overexpression group.Conclusion Overexpressing p55PIK promotes angiogenesis by enhancing VEGF expression in tumor cells,which increases tumorigenesis eventually.
