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<p>Renal cell carcinoma (RCC) is a common malignancy that is often resistant to conventional therapies. Therefore, exploiting the redox-tunable chemistry of selenium, we designed chiral selenium nanoparticles (Se NPs) with a <i>g</i>-factor of 0.012 at 644 nm wavelength that selectively targeted RCC tissues and responded to the tumor microenvironment. In renal tumor cells experiments, <i>D</i>-Se NPs rapidly depleted intracellular glutathione (GSH) and simultaneously elevated intracellular reactive oxygen species (ROS) by 4.43-fold, resulting in a 9.56-fold reduction in the survival rate of tumor cells, compared with the phosphate-buffered saline (PBS) control. Additionally, interferon-β (IFN-β) secretion was upregulated by 3.88-fold, and immunogenic cell death (ICD) was effectively induced under the same conditions. Mechanistically, the affinity of <i>D</i>-Se NPs for the tumor-associated receptor CD70 was highest, driving preferential tumor-cell internalization, which maximized GSH depletion, upregulated tumor-cell ROS sensitivity, induced mitochondrial damage, and amplified downstream stimulator of interferon genes (STING) activation and IFN-β secretion, thereby producing the most potent cytotoxicity. These results confirm that chiral Se NPs can serve as a platform for precise targeting, generating potent anti-tumor immunity with minimal off-target toxicity, providing a promising strategy for promoting anti-tumor immunity.</p>

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CD70-targeted chiral selenium nanotherapeutics eradicate renal cell carcinoma through synergistic oxidative damage and innate immune activation

  • 期刊论文

  • 发表日期：

    2026年4月29日

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  • Panpan Chen,
  • Yihui Hua,
  • Baimei Shi,
  • Chuanlai Xu,
  • Aihua Qu,
  • Xiaobo Zhang,
  • Hua Kuang,
  • Maozhong Sun

摘要

Renal cell carcinoma (RCC) is a common malignancy that is often resistant to conventional therapies. Therefore, exploiting the redox-tunable chemistry of selenium, we designed chiral selenium nanoparticles (Se NPs) with a g-factor of 0.012 at 644 nm wavelength that selectively targeted RCC tissues and responded to the tumor microenvironment. In renal tumor cells experiments, D-Se NPs rapidly depleted intracellular glutathione (GSH) and simultaneously elevated intracellular reactive oxygen species (ROS) by 4.43-fold, resulting in a 9.56-fold reduction in the survival rate of tumor cells, compared with the phosphate-buffered saline (PBS) control. Additionally, interferon-β (IFN-β) secretion was upregulated by 3.88-fold, and immunogenic cell death (ICD) was effectively induced under the same conditions. Mechanistically, the affinity of D-Se NPs for the tumor-associated receptor CD70 was highest, driving preferential tumor-cell internalization, which maximized GSH depletion, upregulated tumor-cell ROS sensitivity, induced mitochondrial damage, and amplified downstream stimulator of interferon genes (STING) activation and IFN-β secretion, thereby producing the most potent cytotoxicity. These results confirm that chiral Se NPs can serve as a platform for precise targeting, generating potent anti-tumor immunity with minimal off-target toxicity, providing a promising strategy for promoting anti-tumor immunity.