论文部分内容阅读
目的：探讨野生型ｐ５３(ｗｔ ｐ５３)基因对人卵巢癌细胞株的生长抑制作用。方法：利用脂质体介导，将含有人全长ｗｔ－ｐ５３基因ｃＤＮＡ的真核表达载体质粒ｐＣＥＰ４／ｐ５３和空载体质粒ｐＣＥＰ４分别转染卵巢癌ＳＫＯＶ３细胞株，分别命名为ＳＫＯＶ３－ｐＣＥＰ４／ｐ５３细胞(C组)、ＳＫＯＶ３－ｐＣＥＰ４细胞(B组)，另设ＳＫＯＶ３细胞为正常对照组（Ａ组）。观察细胞体外生长情况和凋亡变化。结果：外源性ｐ５３基因在Ｃ组细胞中获表达，细胞生长曲线显示ｐ５３的导入使ＳＫＯＶ３细胞生长受到明显抑制，Ｃ组平均细胞集落数（１８．６±１．８个）少于Ａ组（２４．３±２．２个）和Ｂ组（２２．７±２．６），差异有显著性（Ｐ（005）。ＭＴＴ法检测C组细胞活力明显低于Ａ、Ｂ组。Ｃ组细胞Ｇ０～Ｇ１期百分比（５７．７９％）及凋亡细胞百分比（13．９1％）均高于Ｂ组（４６．０２％、２．０８％）和Ａ组（４３．６２％、０）。结论：ｗｔ－ｐ５３基因可介导ＳＫＯＶ３细胞Ｇ１期停滞和细胞凋亡，抑制细胞体外生长。
Objective: To investigate the growth inhibitory effect of wild-type p53 (wt p53) gene on human ovarian cancer cell lines. Methods: The eukaryotic expression vector pCEP4 / p53 and empty vector pCEP4 containing human full-length wt-p53 gene cDNA were transfected into SKOV3 ovarian cancer cell line by lipofectamine respectively and named as SKOV3-pCEP4 / p53 Cells (group C), SKOV3-pCEP4 cells (group B), and SKOV3 cells as normal control group (group A). Observation of cell growth and apoptosis in vitro changes. Results: The exogenous p53 gene was expressed in group C cells. The cell growth curve showed that the introduction of p53 significantly inhibited the growth of SKOV3 cells. The average number of colony-forming cells in group C (18.6 ± 1.8) was less than that in group A (24.3 ± 2.2) and group B (22.7 ± 2.6), the difference was significant (P (005) .MTT assay showed that the viability of group C was significantly lower than that of group A and group B. Group C The percentage of cells in G0 ~ G1 phase (57.79%) and apoptotic cells (13.91%) were higher than those in group B (46.02%, 2.08%) and group A (43.62% .Conclusion: The wt-p53 gene can mediate G1 arrest and apoptosis in SKOV3 cells and inhibit the growth of SKOV3 cells in vitro.