nm23-H1基因抑制口腔癌细胞的侵袭转移行为机制的实验研究

Study on the Mechanism of nm23-Hl on Suppressing the Invasion and Metastatic Behavior of Oral Cancer Cell

[目的]将nm23-H1导入口腔癌BcaCD885细胞株,观察nm23-H1对BcaCD885细胞株侵袭转移能力的影响,并对相关机制进行分析。[方法]制备高纯度的nm23-H1真核表达质粒,并用阳离子脂质体介导的转染技术,完成转染方法的建立。检测转染前后的NDPKA的表达并观察转染前后细胞的侵袭转移行为能力的变化。[结果]将nm23-H1转染口腔癌细胞,获得了稳定表达,发现BcaCD885细胞株nm23-H1基因的转染前后表达水平有明显差异,实验组和对照组的侵袭细胞相对数目分别为41.1％±1.2％和64.5％±6.3％,趋化运动细胞相对数目为50.0％±6.3％和81.0％±3.9％,实验组的粘附能力也显著降低。[结论]nm23-H1对BcaCD885细胞的侵袭转移能力具有显著抑制作用。

[Objective] To transfect nm23-H1 gene into the BcaCD885 cell lines , and observe whether nm23-H1 can affect the invasion and metastatic behavior of BcaCD885 cell lines. [Methods] nm23-H1 gene was transfected into BcaCD885 cell lines using lipofect technique. The difference in expression of nm23-H1 between transfected and non-transfected cell lines was dectected by immunohisto-chemistry. The difference of invision and metastatic behavior was detected by transwell-room and wash way methods. [Results] Stable expression of nm23-H1 was achived by using PCMV-NEO-BAM system. Significant difference in NDPKA expression between transfected and non-transfected of BcaCD885 cell lines was founded; The cell control number of transfected and non-transfected cells which showed the ability of invasion was 41. 1% ± 1. 2% and 64. 5%±6. 3% respectively, while the chemical-trend moving ability was 50. 0% ± 6. 3% and81. 0% ± 3. 9%. The adhesion ability of transfected BcaCD885 cell lines decreased significantly. [Conclusion] nm23-H1 can significant inhibit the metastases of BcaCD885 cell lines.