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BRAK/CXCL14 expression in oral carcinoma cells completely suppresses tumor cell xenografts in SCID mouse

机译:BRAK / CXCL14在口腔癌细胞中的表达完全抑制SCID小鼠中的肿瘤细胞异种移植

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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.
机译:SCID小鼠是人类严重的合并免疫缺陷疾病的模型,除T细胞功能外,B细胞功能也不足。来自其他物种的肿瘤很容易移植到SCID小鼠中,并且会生长而不会被拒绝。我们先前曾报道趋化因子BRAK / CXCL14在正常细胞中表达,但其表达在体外癌症进展模型中被下调,表明它具有抗肿瘤活性。在这里,我们报告说,即使模拟载体引入的对照肿瘤细胞在100%患肿瘤的动物中生长良好,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也被完全抑制(100%)。另外,与T细胞功能缺陷的裸鼠相比,SCID小鼠的异种移植抑制更快,且发生率更高。这些数据表明BRAK表达通过调节肿瘤干细胞与NK细胞之间的相互作用和/或抑制肿瘤微血管形成而抑制肿瘤细胞建立的可能性。

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