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目的将反义CDK4导入人结肠癌细胞株HT29细胞,观察其对肿瘤细胞生长的影响。方法采用lipofectam ine转染方法转染HT29细胞,Northern印迹,W estern印迹,形态学和流式细胞术等方法用于转染效果的鉴定。结果转化细胞有反义CDK4的表达,而内源性CDK4 mRNA表达和蛋白合成下调,并且转化细胞的恶性行为及表型部分逆转,细胞生长受到抑制、软琼脂集落形成能力明显降低,同时揭示G1期阻滞。HT29-asCDK4细胞有较高的凋亡率。结论反义CDK4基因可抑制HT29细胞的生长和增殖、诱导其凋亡。为结直肠癌的基因治疗提供了一种新的可能的途径。
Objective To introduce antisense CDK4 into human colon cancer cell line HT29 and observe its effect on tumor cell growth. Methods Lipofectamine transfection was used to transfect HT29 cells, Northern blot, Western blot, morphological and flow cytometry methods for the identification of transfection results. Results The expression of CDK4 was down-regulated in the transformed cells, but the endogenous CDK4 mRNA and protein synthesis were down-regulated. The malignant behavior and phenotype of the transformed cells were partially reversed. The cell growth was inhibited and the colony-forming ability of the soft agar was significantly reduced. Period of block. HT29-asCDK4 cells have a higher rate of apoptosis. Conclusion Antisense CDK4 gene can inhibit the growth and proliferation of HT29 cells and induce its apoptosis. For colorectal cancer gene therapy provides a new possible way.