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Summary <p>Rana-2PN, identified as the first member of the Ranatuerin antimicrobial peptide family, has been reported to exhibit lipopolysaccharide neutralization, anti-inflammatory effects, and broad-spectrum antimicrobial properties. Besides these biological activities, the potential interactions and effects of this compound on cancer cell lines remain unexplored. In this study, our results indicate that Rana-2PN inhibits the proliferation of K562 cells (IC₅₀ = 4.52 μΜ) and induces significant morphological changes. Flow cytometric analysis using FITC-labeled Rana-2PN revealed its concentration-dependent binding to K562 cells. Furthermore, Rana-2PN treatment upregulated the mRNA expression of key necroptosis markers RIPK1, RIPK3, and MLKL, as quantified by RT-PCR, and promoted necroptotic cell death, which was confirmed by Annexin V-FITC/PI staining and partially inhibited by necrostatin-1. Mechanistically, Rana-2PN induced mitochondrial dysfunction, evidenced by loss of mitochondrial membrane potential (detected by JC-1 staining) and increased mitochondrial permeability (measured by Calcein-AM assay), accompanied by concentration-dependent ROS accumulation (using DCFH-DA staining). In summary, our study provides the possibility of future development of Rana-2PN as a novel therapeutic candidate for the treatment of chronic myelogenous leukemia, particularly in cases where resistance to conventional therapies may develop.</p>

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Rana-2PN, the First Ranatuerin Antimicrobial Peptide, is Associated with Necroptosis Through Mitochondrial Dysfunction and ROS Accumulation in K562 Leukemia Cells

  • 期刊论文

  • 发表日期：

    2025年11月17日

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  • Maolin Tian,
  • Lixia Shu,
  • Jinwei Chai,
  • Tienthanh Nguyen,
  • Xin Chen,
  • Xueqing Xu

摘要

Summary

Rana-2PN, identified as the first member of the Ranatuerin antimicrobial peptide family, has been reported to exhibit lipopolysaccharide neutralization, anti-inflammatory effects, and broad-spectrum antimicrobial properties. Besides these biological activities, the potential interactions and effects of this compound on cancer cell lines remain unexplored. In this study, our results indicate that Rana-2PN inhibits the proliferation of K562 cells (IC₅₀ = 4.52 μΜ) and induces significant morphological changes. Flow cytometric analysis using FITC-labeled Rana-2PN revealed its concentration-dependent binding to K562 cells. Furthermore, Rana-2PN treatment upregulated the mRNA expression of key necroptosis markers RIPK1, RIPK3, and MLKL, as quantified by RT-PCR, and promoted necroptotic cell death, which was confirmed by Annexin V-FITC/PI staining and partially inhibited by necrostatin-1. Mechanistically, Rana-2PN induced mitochondrial dysfunction, evidenced by loss of mitochondrial membrane potential (detected by JC-1 staining) and increased mitochondrial permeability (measured by Calcein-AM assay), accompanied by concentration-dependent ROS accumulation (using DCFH-DA staining). In summary, our study provides the possibility of future development of Rana-2PN as a novel therapeutic candidate for the treatment of chronic myelogenous leukemia, particularly in cases where resistance to conventional therapies may develop.