BRAK/CXCL14 expression in oral carcinoma cells completely suppresses tumor cell xenografts in SCID mouse
BRAK/CXCL14 expression in oral carcinoma cells completely suppresses tumor cell xenografts in SCID mouse
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DOI：
10.2220/biomedres.30.315
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发表时间：
2009-10-01
影响因子：
1.2
通讯作者：
Hata, Ryu-Ichiro
中科院分区：
文献类型：
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作者：
Ozawa, Shigeyuki;Kato, Yasumasa;Hata, Ryu-Ichiro
SCID小鼠是人类严重联合免疫缺陷病的模型，除了T细胞功能外，还缺乏B细胞功能。来自其他物种的肿瘤很容易移植到 SCID 小鼠体内，并且可以在不被排斥的情况下生长。我们之前报道趋化因子 BRAK/CXCL14 在正常细胞中表达，但其表达在体外癌症进展模型中下调，表明其具有抗肿瘤活性的潜力。在这里，我们报告说，在 SCID 小鼠异种移植物中，BRAK/CXCL14 表达载体转染的口腔癌细胞的生长被完全（100%）抑制，尽管引入模拟载体的对照肿瘤细胞生长良好，并且 100% 的动物发生肿瘤。此外，SCID小鼠对异种移植物的抑制速度比T细胞功能缺陷的裸鼠快得多，抑制率也高得多。这些数据表明BRAK表达可能通过调节肿瘤干细胞和NK细胞之间的相互作用和/或抑制肿瘤微血管的形成来抑制肿瘤细胞的建立。
SCID mice are a model of human severe combined immunodeficiency disease and are deficient in B cell function in addition to T cell function. Tumors from other species are easily transplanted into SCID mice and will grow without being rejected. We previously reported that the chemokine BRAK/CXCL14 is expressed in normal cells but its expression is down regulated in an in vitro cancer progression model, suggesting that it has the potential for antitumor activity. Here we report that the growth of BRAK/CXCL14 expression vector-transfected oral cancer cells was completely (100%) suppressed in SCID mouse xenografts even though mock-vector introduced control tumor cells grew well with 100% of animals developing tumors. In addition, suppression of xenografts was Much faster and the rate was much higher in SCID mice than in T cell function-deficient nude mice. These data indicate the possibility that BRAK expression inhibits tumor cell establishment by regulating interactions between tumor stem cells and NK cells and/or suppressing formation of tumor microvessels.