摘要
背景与目的:p53基因为抑癌基因,血管生长抑素(angiostatin,Angio,AS)基因能抑制血管内皮细胞生长和血管新生,间接抑制肿瘤的生长。本研究探讨以pVITRO2质粒为载体共转染野生型人p53和人Angio基因(pVITRO2-hp53-hAngio)对人胃癌细胞生长的影响。方法:用脂质体转染法将pVITRO2-hp53-hAngio转染人胃癌细胞系SG7901。以RT-PCR法检测转染后细胞目的基因的表达,通过细胞集落形成试验、MTT生长曲线、流式细胞仪调亡检测观察其生物学特性变化。结果:野生型p53基因或AS基因转染后均能抑制转染细胞的生长(细胞集落形成试验及MMT,P<0.05),而共转染两种基因的细胞生长抑制诱导凋亡效果优于单个基因转染(细胞集落形成试验及MMT,P<0.05)。结论:p53和AS基因具有协同抑制肿瘤细胞生长作用,提示联合基因可能有利于肿瘤的基因治疗。
Background and purpose: p53 is a kind of antioncogene. Anginstatin( Augio. AS) gene can inhihit the growth of the vascular endothelial cells and the genesis of the vessels. So they could inhibit the growth of the tumor indirectly. We investigated the co-operative suppression of p53 and AS gene in the inhibition of SG7901. Methods: Transfect the pV1TRO2-hp53-hAngio into SG7901 with lipofectamine2000. After transfection . RT-PCR were used to verify whether the target gene had been transfeeted and expressed or not . Cell clones trial. MTT growth curve, flow cytometry assay were used to analyze the results. Results: The cells were suppressed by the two genes and ,inhibition of the combined genes was more powerful than a single one (Clone trial and MTT: P 〈 0.05). Conclusions: The effect of combined genes pV1TRO2-hp53- hAngio on SG7901 is stronger than either one alone.
出处
《中国癌症杂志》
CAS
CSCD
2006年第10期848-850,共3页
China Oncology
基金
福建省自然科学基金资助项目(项目编号C0310017)