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<p>Reactive oxygen species (ROS) in the tumor microenvironment (TME) are key factors involved in inhibiting tumor cell proliferation. This study developed a hollow mesoporous silica-Prussian blue (HMSNs-PB) nanozyme delivery platform loaded with metformin (HPB@MET), which enhances ROS levels within tumor cells through peroxidase-like (POD) activity. Moreover, in the acidic microenvironment of tumors, HPB@MET disintegrates, and the released MET causes mitochondrial dysfunction and increased electron leakage, ultimately promoting the abnormal accumulation of ROS in the TME. In vitro experiments demonstrate that HPB@MET achieves peak cellular uptake at 72&#xa0;h and significantly inhibits tumor cell proliferation through its exceptional ROS-generating capacity. In the K7M2 osteosarcoma model (initial tumor volume 80 mm<sup>3</sup>), HPB@MET increased the tumor inhibition rate from 55% with HPB to 76.5%, with median survival extended to 57 days, indicating that HPB@MET synergistically suppresses tumor cell proliferation via POD activity and mitochondrial dysfunction, effectively suppressing osteosarcoma progression. These results indicate that this nanozyme-drug delivery platform can synergistically promote ROS generation in the TME, effectively inhibiting OS and providing a key technological approach for the efficient treatment of this disease.</p>

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Tumor microenvironment-activated ROS enhancers for effective inhibition of osteosarcoma

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年11月5日

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  • Ke Li,
  • Yufan Huang,
  • Chunmei Xiu

摘要

Reactive oxygen species (ROS) in the tumor microenvironment (TME) are key factors involved in inhibiting tumor cell proliferation. This study developed a hollow mesoporous silica-Prussian blue (HMSNs-PB) nanozyme delivery platform loaded with metformin (HPB@MET), which enhances ROS levels within tumor cells through peroxidase-like (POD) activity. Moreover, in the acidic microenvironment of tumors, HPB@MET disintegrates, and the released MET causes mitochondrial dysfunction and increased electron leakage, ultimately promoting the abnormal accumulation of ROS in the TME. In vitro experiments demonstrate that HPB@MET achieves peak cellular uptake at 72 h and significantly inhibits tumor cell proliferation through its exceptional ROS-generating capacity. In the K7M2 osteosarcoma model (initial tumor volume 80 mm3), HPB@MET increased the tumor inhibition rate from 55% with HPB to 76.5%, with median survival extended to 57 days, indicating that HPB@MET synergistically suppresses tumor cell proliferation via POD activity and mitochondrial dysfunction, effectively suppressing osteosarcoma progression. These results indicate that this nanozyme-drug delivery platform can synergistically promote ROS generation in the TME, effectively inhibiting OS and providing a key technological approach for the efficient treatment of this disease.