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目的研究pp32在前列腺癌细胞中的作用。方法将本实验室先前保存的pcDNA3.1和pcDNA3.1-pp32质粒,转染至Pc3M细胞,构建Pc3M-pp32稳定细胞株。吉姆萨染色实验观察Pc3M细胞的形态变化,通过Transwell小室法检测细胞迁移能力。黏附测定实验鉴定细胞的黏附能力,采用MTT法测定细胞生长曲线。最后,Western印迹检测N-钙黏蛋白(N-cadherin)在细胞中的表达。结果成功筛选并获得了稳定过表达pp32的细胞株(Pc3M-pp32),pp32能引起Pc3M细胞形状的显著改变,引起人前列腺癌细胞Pc3M迁移和黏附能力的增加,明显促进Pc3M细胞的生长,并有效抑制N-钙黏蛋白在Pc3M细胞中的表达。结论过表达pp32可引起Pc3M细胞的形状改变,并可促进Pc3M细胞的迁移、黏附以及生长。
Objective To study the role of pp32 in prostate cancer cells. Methods Plasmids pcDNA3.1 and pcDNA3.1-pp32 previously preserved in our laboratory were transfected into Pc3M cells to construct Pc3M-pp32 stable cell lines. The morphological changes of Pc3M cells were observed by Giemsa staining, and the cell migration ability was detected by Transwell chamber method. Adhesion assay experiments to identify cell adhesion, MTT assay cell growth curve. Finally, Western blotting was used to detect the expression of N-cadherin in the cells. Results The cell line (Pc3M-pp32) overexpressing pp32 was successfully screened and pp32 could induce a significant change in the shape of Pc3M cells, resulting in an increase of Pc3M migration and adhesion in human prostate cancer cells, significantly promoting the growth of Pc3M cells Effectively inhibit the expression of N-cadherin in Pc3M cells. Conclusion Overexpression pp32 can cause the change of shape of Pc3M cells and promote the migration, adhesion and growth of Pc3M cells.