Development of Aptamer-DNAzyme based metal-nucleic acid frameworks for gastric cancer therapy

Jiaqi Yan, Rajendra Bhadane, Meixin Ran, Xiaodong Ma, Yuanqiang Li, Dongdong Zheng, Outi M. H. Salo-Ahen and Hongbo Zhang ()
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Jiaqi Yan: Department of Orthopaedics Shanghai Key Laboratory for Prevention and Treatment of Bone and Joint Diseases Shanghai Institute of Traumatology and Orthopaedics Ruijin Hospital Shanghai Jiao Tong University School of Medicine 197 Ruijin 2nd Road
Rajendra Bhadane: Åbo Akademi University
Meixin Ran: Åbo Akademi University
Xiaodong Ma: Åbo Akademi University
Yuanqiang Li: Åbo Akademi University
Dongdong Zheng: Fudan University Shanghai Cancer Center
Outi M. H. Salo-Ahen: Åbo Akademi University
Hongbo Zhang: Department of Orthopaedics Shanghai Key Laboratory for Prevention and Treatment of Bone and Joint Diseases Shanghai Institute of Traumatology and Orthopaedics Ruijin Hospital Shanghai Jiao Tong University School of Medicine 197 Ruijin 2nd Road

Nature Communications, 2024, vol. 15, issue 1, 1-20

Abstract: Abstract The metal-nucleic acid nanocomposites, first termed metal-nucleic acid frameworks (MNFs) in this work, show extraordinary potential as functional nanomaterials. However, thus far, realized MNFs face limitations including harsh synthesis conditions, instability, and non-targeting. Herein, we discover that longer oligonucleotides can enhance the synthesis efficiency and stability of MNFs by increasing oligonucleotide folding and entanglement probabilities during the reaction. Besides, longer oligonucleotides provide upgraded metal ions binding conditions, facilitating MNFs to load macromolecular protein drugs at room temperature. Furthermore, longer oligonucleotides facilitate functional expansion of nucleotide sequences, enabling disease-targeted MNFs. As a proof-of-concept, we build an interferon regulatory factor-1(IRF-1) loaded Ca2+/(aptamer-deoxyribozyme) MNF to target regulate glucose transporter (GLUT-1) expression in human epidermal growth factor receptor-2 (HER-2) positive gastric cancer cells. This MNF nanodevice disrupts GSH/ROS homeostasis, suppresses DNA repair, and augments ROS-mediated DNA damage therapy, with tumor inhibition rate up to 90%. Our work signifies a significant advancement towards an era of universal MNF application.

Date: 2024
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DOI: 10.1038/s41467-024-48149-9

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