State Key Laboratory of Cancer Biology, Xijing Hospital of Digestive Diseases, The Fourth Military Medical University, Xi'an 710032, Shaanxi Province, PR China.
Biochem Biophys Res Commun. 2010 Mar 19;393(4):788-93. doi: 10.1016/j.bbrc.2010.02.083. Epub 2010 Feb 18.
Our previous study revealed that human ribosomal protein L6 (RPL6) was upregulated in multidrug-resistant gastric cancer cells and over-expression of RPL6 could protect gastric cancer cells from drug-induced apoptosis. The present study was designed to explore the role of RPL6 in tumorigenesis and development of gastric cancer. The expression of RPL6 in gastric cancer tissues and normal gastric mucosa was evaluated by immunohistochemical staining. It was found RPL6 was expressed at a higher level in gastric cancer tissues than that in normal gastric mucosa. RPL6 was then genetically overexpressed or knocked down in human immortalized gastric mucosa epithelial GES cells. It was demonstrated that upregulation of RPL6 accelerated the growth and enhanced in vitro colony forming ability of GES cells whereas downregulation of RPL6 showed adverse effects. Moreover, over-expression of RPL6 could promote G1 to S phase transition of GES cells. It was further evidenced that upregulation of RPL6 resulted in elevated cyclin E expression while downregulation of RPL6 caused decreased cyclin E expression in GES cells. Taken together, these data indicated that RPL6 was overexpressed in human gastric cancer and its over-expression could promote cell growth and cell cycle progression at least through upregulating cyclin E expression.
我们之前的研究表明，人类核糖体蛋白 L6（RPL6）在多药耐药性胃癌细胞中上调，并且 RPL6 的过表达可以保护胃癌细胞免受药物诱导的细胞凋亡。本研究旨在探讨 RPL6 在胃癌发生和发展中的作用。通过免疫组织化学染色评估 RPL6 在胃癌组织和正常胃黏膜中的表达。结果发现，RPL6 在胃癌组织中的表达水平高于正常胃黏膜。然后在人永生化胃黏膜上皮 GES 细胞中过表达或敲低 RPL6。结果表明，RPL6 的上调加速了 GES 细胞的生长并增强了其体外集落形成能力，而 RPL6 的下调则产生了相反的效果。此外，RPL6 的过表达可促进 GES 细胞从 G1 期向 S 期的转变。进一步的证据表明，RPL6 的上调导致细胞周期蛋白 E 的表达升高，而 RPL6 的下调导致 GES 细胞中细胞周期蛋白 E 的表达降低。综上所述，这些数据表明 RPL6 在人胃癌中过表达，其过表达至少可以通过上调细胞周期蛋白 E 的表达来促进细胞生长和细胞周期进程。
