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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 & OBJECTIVE: The p53 gene is a tumor suppressor gene. Angiostatin (Angio, AS) gene can inhibit the growth of vascular endothelial cells and angiogenesis and indirectly inhibit tumor growth. This study was to investigate the effect of pVITRO2 plasmid co-transfecting wild-type human p53 and human Angio gene (pVITRO2-hp53-hAngio) on the growth of human gastric cancer cells. Methods: pVITRO2-hp53-hAngio was transfected into human gastric cancer cell line SG7901 by lipofection. The gene expression of the transfected cells was detected by RT-PCR. The changes of the biological characteristics were observed by cell colony formation assay, MTT growth curve and apoptosis assay by flow cytometry. RESULTS: Transfection of wild-type p53 gene or AS gene inhibited the growth of transfected cells (colony formation assay and MMT, P <0.05), while the cotransfection of both genes inhibited cell growth and induced apoptosis better than Single gene transfection (colony formation assay and MMT, P <0.05). Conclusion: p53 and AS genes can inhibit the growth of tumor cells synergistically, suggesting that the combined gene may be beneficial to tumor gene therapy.