BRAK/CXCL14 expression suppresses tumor growth in vivo in human oral carcinoma cells
BRAK/CXCL14 expression suppresses tumor growth in vivo in human oral carcinoma cells
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DOI：
10.1016/j.bbrc.2006.07.070
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发表时间：
2006-09-22
影响因子：
3.1
通讯作者：
Hata, Ryu-Ichiro
中科院分区：
文献类型：
--
作者：
Ozawa, Shigeyuki;Kato, Yasumasa;Hata, Ryu-Ichiro
为了找到口腔癌 (OC) 体内肿瘤进展的抑制因子，我们寻找用表皮生长因子 (EGF) 处理 OC 细胞时下调的分子，表皮生长因子 (EGF) 的受体在 OC 中经常过度激活。通过 cDNA 微阵列分析和逆转录酶聚合酶链反应分析观察到，用 EGF 处理 OC 细胞后，BRAK（也称为 CXC 趋化因子配体 14 (CXCL14)）的表达显着下调。 EGF 效应因 MEK 抑制剂的共存而减弱。表达BRAK的载体转染的无胸腺裸鼠肿瘤细胞体内成瘤率显着低于转染模拟载体的肿瘤细胞。此外，表达 BRAK 的细胞在体内形成的肿瘤明显小于模拟转染细胞的肿瘤。这些结果表明BRAK/CXCL14是一种趋化因子，对体内OC的肿瘤进展具有抑制活性。 (c) 2006 Elsevier Inc. 保留所有权利。
In order to find a suppressor(s) of tumor progression in vivo for oral carcinoma (OC), we searched for molecules down-regulated in OC cells when the cells were treated with epidermal growth factor (EGF), whose receptor is frequently over-activated in OC. The expression of BRAK, which is also known as CXC chemokine ligand14 (CXCL14), was down-regulated significantly by the treatment of OC cells with EGF as observed by cDNA microarray analysis followed by reverse-transcriptase polymerase chain reaction analysis. The EGF effect was attenuated by the co-presence of a MEK inhibitor. The rate of tumor formation in vivo of BRAK-expressing vector-transfected tumor cells in athymic nude mice was significantly lower than that of mock vector-transfected ones. In addition tumors formed in vivo by the BRAK-expressing cells were significantly smaller than those of the mock-transfected ones. These results indicate that BRAK/CXCL14 is a chemokine, having suppressive activity toward tumor progression of OC in vivo. (c) 2006 Elsevier Inc. All rights reserved.