Hunt Hannah L, Goncalves Beatriz G, Biggs Mary A, Rico Mia I, Murray Molly E, Lebedenko Charlotta G, Banerjee Ipsita A
Department of Chemistry, Fordham University, 441 East Fordham Road, Bronx, NY, 10458, USA.
Mol Divers. 2024 Dec;28(6):3683-3711. doi: 10.1007/s11030-023-10772-x. Epub 2024 Jan 19.
Peptide-based therapeutics have been gaining attention due to their ability to actively target tumor cells. Additionally, several varieties of nucleotide derivatives have been developed to reduce cell proliferation and induce apoptosis of tumor cells. In this work, we have developed novel peptide conjugates with newly designed purine analogs and pyrimidine derivatives and explored the binding interactions with the kinase domain of wild-type EGFR and its mutant EGFR [L858R/ T790M] which are known to be over-expressed in tumor cells. The peptides explored included WNWKV (derived from sea cucumber) and LARFFS, which in previous work was predicted to bind to Domain I of EGFR. Computational studies conducted to explore binding interactions include molecular docking studies, molecular dynamics simulations and MMGBSA to investigate the binding abilities and stability of the complexes. The results indicate that conjugation enhanced binding capabilities, particularly for the WNWKV conjugates. MMGBSA analysis revealed nearly twofold higher binding toward the T790M/L858R double mutant receptor. Several conjugates were shown to have strong and stable binding with both wild-type and mutant EGFR. As a proof of concept, we synthesized pyrimidine conjugates with both peptides and determined the KD values using SPR analysis. The results corroborated with the computational analyses. Additionally, cell viability and apoptosis studies with lung cancer cells expressing the wild-type and double mutant proteins revealed that the WNWKV conjugate showed greater potency than the LARFFS conjugate, while LARFFS peptide alone showed poor binding to the kinase domain. Thus, we have designed peptide conjugates that show potential for further laboratory studies for developing therapeutics for targeting the EGFR receptor and its mutant T790M/L858R.
基于肽的疗法因其能够主动靶向肿瘤细胞而受到关注。此外,已经开发了几种核苷酸衍生物以减少细胞增殖并诱导肿瘤细胞凋亡。在这项工作中,我们开发了与新设计的嘌呤类似物和嘧啶衍生物的新型肽缀合物,并探索了与野生型EGFR及其突变体EGFR [L858R/T790M]的激酶结构域的结合相互作用,已知这些在肿瘤细胞中过表达。所探索的肽包括WNWKV(源自海参)和LARFFS,在先前的工作中预测其与EGFR的结构域I结合。为探索结合相互作用而进行的计算研究包括分子对接研究、分子动力学模拟和MMGBSA,以研究复合物的结合能力和稳定性。结果表明缀合增强了结合能力,特别是对于WNWKV缀合物。MMGBSA分析显示对T790M/L858R双突变受体的结合几乎高出两倍。几种缀合物显示与野生型和突变型EGFR都有强而稳定的结合。作为概念验证,我们合成了与两种肽的嘧啶缀合物,并使用SPR分析确定了KD值。结果与计算分析一致。此外,对表达野生型和双突变蛋白的肺癌细胞进行的细胞活力和凋亡研究表明,WNWKV缀合物比LARFFS缀合物表现出更大的效力,而单独的LARFFS肽与激酶结构域的结合较差。因此,我们设计的肽缀合物显示出在进一步实验室研究中开发靶向EGFR受体及其突变体T790M/L858R的疗法的潜力。