Neoplasma. 2016;63(3):385-93. doi: 10.4149/307_150822N455.
The objective of the study was to investigate the impact of BTG2 on growth, migration and invasion of human clear cell renal cell carcinoma (ccRCC) cells. Endogenous expression of BTG2 was evaluated in the ccRCC cell lines (Caki-1, 786-O and Caki-2) and noncancerous human renal proximal tubular cell lines (HKC, HK-2 and RPTEC). BTG2 expression was decreased in the ccRCC cells compared with the noncancerous cells (P < 0.01). Then Caki-1 and 786-O cells described as suitable transfection hosts were used in transfection to carry out biological function studies. The three experimental groups were as follows: BTG2-ORF (transfected with BTG2-ORF plasmid), blank-Vector (transfected with pCMV6-Entry), and Cell-alone group (no DNA transfected in). BTG2 expression in the BTG2-ORF groups was significantly higher than that in the controls (P < 0.01). Cell growth was remarkably reduced and the number of migrating or invading cells was reduced in the BTG2-ORF groups compared with the controls (P < 0.01). Furthermore, Matrix Metalloproteinase-9 (MMP-9), Cyclin D1 and Cyclin E expression were reduced in the BTG2-ORF groups compared with the controls. Here, we have provided data for attenuated BTG2 expression in the ccRCC cells. Overexpressed BTG2 could inhibit cell proliferation, migration and invasion of human ccRCC, and the suppressive effects might be due to down-regulation of MMP-9, Cyclin D1 and Cyclin E expression.
本研究旨在探讨 BTG2 对人肾透明细胞癌细胞（ccRCC）生长、迁移和侵袭的影响。评估了 ccRCC 细胞系（Caki-1、786-O 和 Caki-2）和非癌细胞人肾近端小管细胞系（HKC、HK-2 和 RPTEC）中的内源性 BTG2 表达。与非癌细胞相比，ccRCC 细胞中的 BTG2 表达降低（P < 0.01）。然后，选用 Caki-1 和 786-O 细胞作为合适的转染宿主进行转染，以开展生物学功能研究。三个实验组如下：BTG2-ORF（转染 BTG2-ORF 质粒）、空白载体（转染 pCMV6-Entry）和细胞对照组（未转染 DNA）。BTG2-ORF 组的 BTG2 表达明显高于对照组（P < 0.01）。BTG2-ORF 组细胞生长明显减少，迁移或侵袭细胞数量减少，与对照组相比（P < 0.01）。此外，BTG2-ORF 组的基质金属蛋白酶-9（MMP-9）、周期蛋白 D1 和周期蛋白 E 的表达均低于对照组。在此，我们提供了 ccRCC 细胞中 BTG2 表达减弱的数据。过表达 BTG2 可抑制人 ccRCC 细胞的增殖、迁移和侵袭，抑制作用可能是由于 MMP-9、周期蛋白 D1 和周期蛋白 E 表达下调所致。
