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首页> 外文期刊>Cancer science. >Antitumor effect of nuclear factor-κB decoy transfer by mannose-modified bubble lipoplex into macrophages in mouse malignant ascites
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Antitumor effect of nuclear factor-κB decoy transfer by mannose-modified bubble lipoplex into macrophages in mouse malignant ascites

机译：甘露糖修饰的泡沫脂质复合物将核因子-κB诱饵转移到小鼠恶性腹水中巨噬细胞中的抗肿瘤作用

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Patients with malignant ascites (MAs) display several symptoms, such as dyspnea, nausea, pain, and abdominal tenderness, resulting in a significant reduction in their quality of life. Tumor-associated macrophages (TAMs) play a crucial role in MA progression. Because TAMs have a tumor-promoting M2 phenotype, conversion of the M2 phenotypic function of TAMs would be promising for MA treatment. Nuclear factor-κB (NF-κB) is a master regulator of macrophage polarization. Here, we developed targeted transfer of a NF-κB decoy into TAMs by ultrasound (US)-responsive, mannose-modified liposome/NF-κB decoy complexes (Man-PEG bubble lipoplexes) in a mouse peritoneal dissemination model of Ehrlich ascites carcinoma. In addition, we investigated the effects of NF-κB decoy transfection into TAMs on MA progression and mouse survival rates. Intraperitoneal injection of Man-PEG bubble lipoplexes and US exposure transferred the NF-κB decoy into TAMs effectively. When the NF-κB decoy was delivered into TAMs by this method in the mouse peritoneal dissemination model, mRNA expression of the Th2 cytokine interleukin (IL)-10 in TAMs was decreased significantly. In contrast, mRNA levels of Th1 cytokines (IL-12, tumor necrosis factor-α, and IL-6) were increased significantly. Moreover, the expression level of vascular endothelial growth factor in ascites was suppressed significantly, and peritoneal angiogenesis showed a reduction. Furthermore, NF-κB decoy transfer into TAMs significantly decreased the ascitic volume and number of Ehrlich ascites carcinoma cells in ascites, and prolonged mouse survival. In conclusion, we transferred a NF-κB decoy efficiently by Man-PEG bubble lipoplexes with US exposure into TAMs, which may be a novel approach for MA treatment.
机译：恶性腹水（MAs）患者表现出多种症状，例如呼吸困难，恶心，疼痛和腹部压痛，导致其生活质量显着降低。肿瘤相关巨噬细胞（TAM）在MA进展中起关键作用。因为TAM具有促进肿瘤的M2表型，所以TAM的M2表型功能的转换对于MA治疗很有希望。核因子-κB（NF-κB）是巨噬细胞极化的主要调节因子。在这里，我们开发了通过超声（美国）响应，甘露糖修饰的脂质体/NF-κB诱饵复合物（Man-PEG气泡脂质复合物）在艾氏腹水小鼠腹膜扩散模型中将NF-κB诱饵定向转移到TAM中。此外，我们研究了将NF-κB诱饵转染到TAM中对MA进展和小鼠存活率的影响。腹膜内注射Man-PEG泡沫脂质复合物和美国暴露使NF-κB诱饵有效转移到TAM中。当通过这种方法在小鼠腹膜扩散模型中将NF-κB诱饵递送到TAM中时，TAM中Th2细胞因子白介素（IL）-10的mRNA表达显着降低。相反，Th1细胞因子（IL-12，肿瘤坏死因子-α和IL-6）的mRNA水平显着增加。此外，腹水中血管内皮生长因子的表达水平被显着抑制，腹膜血管生成减少。此外，NF-κB诱饵转移到TAM中显着降低了腹水中Ehrlich腹水癌细胞的腹水量和数量，并延长了小鼠的存活时间。总之，我们通过Man-PEG泡状脂质复合物在美国暴露于TAM中有效地转移了NF-κB诱饵，这可能是MA治疗的一种新方法。

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