Department of Pathobiology, College of Veterinary Medicine, Auburn University, Auburn, AL 36849, USA.
Protein Eng Des Sel. 2012 Jun;25(6):271-83. doi: 10.1093/protein/gzs013. Epub 2012 Apr 6.
Breast cancer is a leading cause of death among women in the USA. The efficacy of existing anticancer therapeutics can be improved by targeting them through conjugation with ligands binding to cellular receptors. Recently, we developed a novel drug targeting strategy based on the use of pre-selected cancer-specific 'fusion pVIII proteins' (fpVIII), as targeting ligands. To study the efficiency of this approach in animal models, we developed a panel of breast cancer cell-binding phages as a source of targeted fpVIIIs. Two landscape phage peptide libraries (8-mer f8/8 and 9-mer f8/9) were screened to isolate 132 phage variants that recognize breast carcinoma cells MCF-7 and ZR-75-1 and internalize into the cells. When tested for their interaction with the breast cancer cells in comparison with liver cancer cells HepG2, human mammary cells MCF-10A cells and serum, 16 of the phage probes selectively interacted with the breast cancer cells whereas 32 bound both breast and liver cancer cells. The most prominent cancer-specific phage DMPGTVLP, demonstrating sub-nanomolar Kd in interaction with target cells, was used for affinity chromatography of cellular membrane molecules to reveal its potential binding receptor. The isolated protein was identified by direct sequencing as cellular surface nucleolin. This conclusion was confirmed by inhibition of the phage-cell interaction with nucleolin antibodies. Other prominent phage binders VPTDTDYS, VEEGGYIAA, and DWRGDSMDS demonstrate consensus motifs common to previously identified cancer-specific peptides. Isolated phage proteins exhibit inherent binding specificity towards cancer cells, demonstrating the functional activity of the selected fused peptides. The selected phages, their peptide inserts and intact fusion proteins can serve as promising ligands for the development of targeted nanomedicines and their study in model mice with xenograft of human cells MCF-7 and ZR-75-1.
乳腺癌是美国女性死亡的主要原因之一。通过与结合细胞受体的配体结合对现有抗癌疗法进行靶向,可以提高其疗效。最近,我们开发了一种新的药物靶向策略,基于使用预先选择的癌症特异性“融合 pVIII 蛋白”(fpVIII)作为靶向配体。为了在动物模型中研究这种方法的效率,我们开发了一组乳腺癌细胞结合噬菌体作为靶向 fpVIIIs 的来源。筛选了两个景观噬菌体肽文库(8-mer f8/8 和 9- mer f8/9),以分离 132 个识别乳腺癌细胞 MCF-7 和 ZR-75-1 并内化进入细胞的噬菌体变体。当将其与肝癌细胞 HepG2、人乳腺细胞 MCF-10A 细胞和血清中的乳腺癌细胞进行比较时,16 个噬菌体探针选择性地与乳腺癌细胞相互作用,而 32 个探针与乳腺癌和肝癌细胞都结合。最突出的癌症特异性噬菌体 DMPGTVLP 与靶细胞相互作用的 Kd 值低于纳摩尔,用于亲和层析细胞膜分子以揭示其潜在的结合受体。通过直接测序鉴定出分离的蛋白质是细胞表面核仁素。用核仁素抗体抑制噬菌体-细胞相互作用证实了这一结论。其他突出的噬菌体结合物 VPTDTDYS、VEEGGYIAA 和 DWRGDSMDS 展示了与先前鉴定的癌症特异性肽共同的保守基序。分离的噬菌体蛋白对癌细胞表现出固有结合特异性,证明了所选融合肽的功能活性。所选噬菌体、其肽插入物和完整融合蛋白可作为有前途的配体,用于开发靶向纳米药物,并在 MCF-7 和 ZR-75-1 人细胞异种移植的模型小鼠中进行研究。