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将互补于C-m yc mRNA的反义寡核苷酸(A SON)进行放射性碘(131I,125I)标记,通过多聚赖氨酸与血管活性肠肽(V IP)偶联形成放射性反义复合物(V IP1-31I-A SON,V IP1-25I-A SON)。以正义(SON)和无义链(M ON)作为对照,比较HT 29结肠癌细胞对125I-A SON和V IP1-25I-A SON的摄取率;利用M TT法和流式细胞计数仪检测C-m yc癌蛋白方法,研究131I-A SON和V IP1-31I-A SON对HT 29结肠癌细胞的作用。实验结果表明,与V IP结合后,125I-A SON在结肠腺癌HT 29细胞中的摄取率大大提高,与未结合125I-A SON摄取率相比差异显著(P<0.05)。V IP1-31I-A SON对HT 29细胞生长抑制作用呈剂量依赖型,且抑制作用显著强于其它各对照组(P<0.05)。流式细胞计数表明,与V IP1-31I-A SON组和131I-A SON组荧光强度明显低于其它各组(P<0.05),而V IP1-31I-A SON组的荧光强度又比131I-A SON组低(P<0.01),表明V IP作为载体,能有效将A SON导入结肠癌细胞,明显抑制HT 29结肠癌细胞的生长和C-m yc癌蛋白的表达。
Antisense oligonucleotides (A SON) complementary to Cm yc mRNA were radioiodinated (131I, 125I) labeled and conjugated to vasoactive intestinal peptide (VIP) via polylysine to form radioactive antisense complexes (VIP1-31I-A SON, VIP1-25I-A SON). The uptake of 125I-A SON and VIP1-25I-A SON by HT29 colon cancer cells was compared with normal (SON) and nonsense (M ON) controls; MTH and flow cytometry Cm yc oncoprotein method to investigate the effects of 131I-A SON and VP1-31I-A SON on HT29 colon cancer cells. The results showed that the uptake of 125I-A SON in colon adenocarcinoma HT 29 cells was greatly increased after binding to V IP, which was significantly different from the unbound 125I-A SON uptake rate (P <0.05). V IP1-31I-A SON inhibited the growth of HT29 cells in a dose-dependent manner, and its inhibitory effect was significantly stronger than that of other control groups (P <0.05). Flow cytometry showed that the fluorescence intensity of VIP1-31I-A SON group and 131I-A SON group was significantly lower than that of other groups (P <0.05), while the fluorescence intensity of VIP1-31I-A SON group was higher than that of 131I -A SON group (P <0.01), indicating that V IP as a carrier, can effectively A SON into colon cancer cells, significantly inhibited HT 29 colon cancer cell growth and Cm yc oncoprotein expression.