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FGF2-丝氨酸蛋白酶融合蛋白通过 PCI 胞质递送在过表达 FGFR1 的细胞中的功效和选择性。

Efficacy and Selectivity of FGF2-Saporin Cytosolically Delivered by PCI in Cells Overexpressing FGFR1.

机构信息

Department of Tumor Biology, Institute for Cancer Research, The Norwegian Radium Hospital, Oslo University Hospital, Montebello, 0379 Oslo, Norway.

Centre for Cancer Cell Reprogramming, Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Montebello, 0379 Oslo, Norway.

出版信息

Cells. 2021 Jun 12;10(6):1476. doi: 10.3390/cells10061476.

Abstract

Fibroblast growth factor receptors (FGFRs) have become an attractive target in cancer research and therapy due to their implication in several cancers. Limitations of current treatment options require a need for additional, more specific and potent strategies to overcome cancers driven by FGFRs. Photochemical internalization (PCI) is a light-controlled method for cytosolic delivery of drugs that are entrapped in endosomes and lysosomes. We here evaluated the efficacy and selectivity of PCI of FGF2-saporin (FGF-SAP) in cells overexpressing FGFR1. FGF-SAP is a conjugate of FGF2 and the highly cytotoxic ribosome-inactivating protein (RIP) saporin, which is used as payload to eliminate cancer cells. Evaluation of the targeting effect of PCI of FGF-SAP was done by comparing the cytotoxic response in osteosarcoma cells with very low levels of FGFR1 (U2OS) to cells overexpressing FGFR1 (U2OS-R1). We demonstrate that PCI greatly enhances cytotoxicity of the drug showing efficient cell killing at pM concentrations of the drug in U2OS-R1 cells. However, U2OS cells were also sensitive to the toxin after PCI. Binding experiments using confocal microscopy and Western blotting techniques indicate that FGF-SAP is taken up by cells through heparan sulfate proteoglycans (HSPGs) in U2OS cells. We further show that the cytotoxicity of FGF-SAP in U2OS cells was reduced when cells were co-treated with heparin to compete out binding to HSPG, demonstrating that the cytotoxic effect was due to internalization by HSPGs. We conclude that to prevent off-target effects of FGF-based toxins, it will be necessary to circumvent binding to HSPGs, for example by mutating the binding site of FGF2 to HSPGs.

摘要

成纤维细胞生长因子受体 (FGFRs) 在几种癌症中发挥作用,因此成为癌症研究和治疗的一个有吸引力的靶点。由于当前治疗方案的局限性,需要额外的、更特异和更强效的策略来克服由 FGFRs 驱动的癌症。光化学内吞作用(PCI)是一种控制细胞内药物传递的方法,可将药物包埋在内体和溶酶体中。我们在此评估了 FGFR1 过表达细胞中 FGF2-蓖麻毒素(FGF-SAP)的 PCI 的疗效和选择性。FGF-SAP 是 FGF2 和高细胞毒性核糖体失活蛋白(RIP)蓖麻毒素的缀合物,用作消除癌细胞的有效载荷。通过比较具有非常低 FGFR1 水平的骨肉瘤细胞(U2OS)和过表达 FGFR1 的细胞(U2OS-R1)中 PCI 的 FGF-SAP 的靶向效果,评估了 PCI 的靶向效果。我们证明 PCI 大大增强了药物的细胞毒性,在 U2OS-R1 细胞中以 pM 浓度的药物即可实现有效的细胞杀伤。然而,U2OS 细胞在 PCI 后也对毒素敏感。使用共聚焦显微镜和 Western blot 技术进行的结合实验表明,FGF-SAP 通过 U2OS 细胞中的硫酸乙酰肝素蛋白聚糖(HSPGs)被细胞摄取。我们进一步表明,当细胞用肝素共同处理以竞争与 HSPG 的结合从而减少细胞内毒素的结合时,FGF-SAP 在 U2OS 细胞中的细胞毒性降低,证明细胞毒性是由于 HSPGs 的内化作用所致。我们得出结论,为了防止基于 FGF 的毒素的脱靶效应,有必要避免与 HSPGs 结合,例如通过突变 FGF2 与 HSPGs 的结合位点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/38d5/8231185/227c2697c980/cells-10-01476-g001.jpg

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