NIR-Activated Hollow Upconversion Nanocomposites for Tumor Therapy via GLUT1 Inhibition and Mitochondrial Function Disruption

  • ACS Appl Mater Interfaces. 2025 Apr 9;17(14):20849-20858. doi: 10.1021/acsami.5c00442.
Yuan Liang  1  2  3 ,  Ran An  3 ,  Pengye Du  3 ,  Yi Wei  3 ,  Shuyu Liu  3 ,  Jianhao Zheng  3 ,  Pengpeng Lei  3 ,  Hongjie Zhang  1  2  3  4
Affiliations
  • 1. School of Rare Earths, University of Science and Technology of China, Anhui, Hefei 230026, China.
  • 2. Ganjiang Innovation Academy, Chinese Academy of Science, Jiangxi, Ganzhou 341000, China.
  • 3. State Key Laboratory of Rare Earth Resource Utilization, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences, Jilin, Changchun 130022, China.
  • 4. Department of Chemistry, Tsinghua University, Beijing 100084, China.
PMID: 40166910 DOI: 10.1021/acsami.5c00442
Abstract

Tumor remains a leading contributor to global mortality rates, necessitating urgent advancements in therapeutic interventions. Due to the intricate nature of the tumor microenvironment, individual differences make it difficult to achieve desired efficacy with a single strategy. To overcome these challenges, we develop for the first time hollow NaBiF4-based nanocomposites NaBiF4-W/R-D for tumor therapy by glucose transporter 1 (GLUT1) inhibition and mitochondrial function disruption. NaBiF4-W/R-D can inhibit GLUT1 function due to the presence of WZB117, which leads to a decrease in intracellular glucose in tumor cells, leaving them in a starved state. Meanwhile, the upconversion luminescence of NaBiF4-W/R-D under near-infrared (NIR) laser irradiation can stimulate the Photosensitizer to efficiently generate singlet oxygen to disrupt the mitochondrial function and then kill the tumor cells. In addition, NIR-II emission from NaBiF4-W/R-D is used for fluorescence imaging to determine the optimal time point for tumor treatment. Finally, NaBiF4-W/R-D leads to mitochondrial membrane potential depolarization, impaired mitochondrial function, activation of Caspase-3, and ultimately the amplification of Apoptosis.

Keywords
GLUT1 inhibition; NIR; hollow; mitochondrial dysfunction; upconversion.
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