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噬菌体在小鼠实验性癌症模型中的抗肿瘤活性可能是由β3整合素信号通路的抑制引起的。

Antitumor activity of bacteriophages in murine experimental cancer models caused possibly by inhibition of beta3 integrin signaling pathway.

作者信息

Dabrowska K, Opolski A, Wietrzyk J, Switala-Jelen K, Boratynski J, Nasulewicz A, Lipinska L, Chybicka A, Kujawa M, Zabel M, Dolinska-Krajewska B, Piasecki E, Weber-Dabrowska B, Rybka J, Salwa J, Wojdat E, Nowaczyk M, Gorski A

机构信息

Institute of Immunology and Experimental Therapy, 53-114 Wroclaw, Poland.

出版信息

Acta Virol. 2004;48(4):241-8.

Abstract

Bacteriophages (phages) as bacterial viruses are generally believed to have no intrinsic tropism for mammalian cells. In this study the interactions between phages and various eukaryotic cells were investigated. Binding of phages to the membranes of cancer and normal blood cells was observed. Moreover, it was shown that the wild-type phage T4 (wtT4) and its substrain HAP1 with enhanced affinity for melanoma cells inhibit markedly and significantly experimental lung metastasis of murine B16 melanoma cells by 47% and 80%, respectively. A possible molecular mechanism of these effects, namely a specific interaction between the Lys-Gly-Asp motif of the phage protein 24 and beta3-integrin receptors on target cells is proposed. It was also shown that anti-beta3 antibodies and synthetic peptides mimicking natural beta3 ligands inhibit the phage binding to cancer cells. This is in line with the well-described beta3 integrin-dependent mechanism of tumor metastasis. It is concluded that the blocking of beta3 integrins by phage preparations results in a significant decrease in tumor invasiveness.

摘要

噬菌体作为细菌病毒,通常被认为对哺乳动物细胞没有内在嗜性。在本研究中,对噬菌体与各种真核细胞之间的相互作用进行了研究。观察到噬菌体与癌细胞和正常血细胞的膜结合。此外,研究表明,野生型噬菌体T4(wtT4)及其对黑色素瘤细胞具有增强亲和力的亚菌株HAP1分别显著抑制小鼠B16黑色素瘤细胞的实验性肺转移47%和80%。提出了这些效应可能的分子机制,即噬菌体蛋白24的Lys-Gly-Asp基序与靶细胞上的β3整合素受体之间的特异性相互作用。研究还表明,抗β3抗体和模拟天然β3配体的合成肽可抑制噬菌体与癌细胞的结合。这与已充分描述的β3整合素依赖性肿瘤转移机制一致。得出的结论是,噬菌体制剂阻断β3整合素会导致肿瘤侵袭性显著降低。

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