Zhang Qiu-Hong, Wu Ming-Hua, Wang Li-Li, Cao Li, Tang Ke, Peng Cong, Gan Kai, Li Xiao-Ling, Li Gui-Yuan
Cancer Research Institute, Central South University, Changsha 410078, China.
Acta Biochim Biophys Sin (Shanghai). 2005 Oct;37(10):680-7. doi: 10.1111/j.1745-7270.2005.00100.x.
Our previous study has shown that LRRC4 is a novel member of the leucine-rich repeat (LRR) superfamily and has the potential to suppress brain tumor growth. In order to further analyze the functions of LRRC4 on the maintenance of normal function and suppression of tumorigenesis in the central nervous system, we investigated alterations in gene expression related to neurobiology by the Atlas array in two inducible dual-stable LRRC4-overexpressing cell lines. Seventeen of 588 genes spotted on the Atlas membrane showed altered expression levels in LRRC4 transfected U251MG Tet-on cells, which are involved in cell proliferation and cell cycle progression, tumor invasion and metastasis, and neurotransmitter synthesis and release. In addition, cell invasion assay results showed that LRRC4 can inhibit the U251MG cell migration. These studies represent the first cDNA array analysis of the effects of LRRC4 on the involvement of different neurobiological genes in U251MG glioblastoma cells and provide new insights into the function of LRRC4 in glioma.
我们之前的研究表明，LRRC4是富含亮氨酸重复序列（LRR）超家族的一个新成员，具有抑制脑肿瘤生长的潜力。为了进一步分析LRRC4在维持中枢神经系统正常功能和抑制肿瘤发生方面的作用，我们通过Atlas芯片研究了两种可诱导的双稳定LRRC4过表达细胞系中与神经生物学相关的基因表达变化。Atlas膜上588个基因中的17个在LRRC4转染的U251MG Tet-on细胞中表达水平发生了改变，这些基因涉及细胞增殖和细胞周期进程、肿瘤侵袭和转移以及神经递质的合成和释放。此外，细胞侵袭试验结果表明，LRRC4可抑制U251MG细胞迁移。这些研究首次对LRRC4对U251MG胶质母细胞瘤细胞中不同神经生物学基因参与情况的影响进行了cDNA芯片分析，并为LRRC4在胶质瘤中的功能提供了新的见解。
