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<p>This work developed and evaluated a crocin-coated zinc–sodium alginate–polyethylene glycol (Zn/SAG/PEG/Cr) nanocomposite as a potential therapeutic against bladder cancer using T24 human carcinoma and Vero kidney epithelial cells. Systematic characterization confirmed successful zinc incorporation, a crystalline inorganic phase, and nanoscale particle size with high compositional purity. MTT assay demonstrated that the nanocomposite exerts selective, concentration-dependent cytotoxicity against T24 cells while maintaining biocompatibility with normal Vero cells. Mechanistic analysis revealed that treatment of the nanocomposite significantly enhanced intracellular reactive oxygen species (ROS) generation, disrupted mitochondrial membrane potential, and compromised plasma membrane integrity. Furthermore, the nanocomposite suppressed pro-inflammatory mediators (TNF-α, NF-κB, COX-2, and IL-6) and induced apoptosis, evidenced by elevated Bax, caspase-3, and caspase-9 levels alongside reduced Bcl-2 expression. Crucially, the formulated nanocomposite attenuated the PI3K/Akt/mTOR signaling pathway, a key regulator of bladder cancer progression. Despite these potent anti-oncogenic effects, challenges remain regarding the precise control of crocin release kinetics and the long-term metabolic clearance of the metallic zinc component. Future prospects involve validating these findings in orthotopic animal models to assess systemic toxicity and optimizing the formulation for targeted intravesical delivery to improve clinical translation.</p>

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Crocin-coated zinc–alginate–PEG nanocomposite induces ROS-mediated apoptosis via PI3K/Akt/mTOR suppression in bladder cancer cells

  • 期刊论文

  • 发表日期：

    2026年6月2日

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  • Yueshan Wang,
  • Sensheng An,
  • Yongzheng Min

摘要

This work developed and evaluated a crocin-coated zinc–sodium alginate–polyethylene glycol (Zn/SAG/PEG/Cr) nanocomposite as a potential therapeutic against bladder cancer using T24 human carcinoma and Vero kidney epithelial cells. Systematic characterization confirmed successful zinc incorporation, a crystalline inorganic phase, and nanoscale particle size with high compositional purity. MTT assay demonstrated that the nanocomposite exerts selective, concentration-dependent cytotoxicity against T24 cells while maintaining biocompatibility with normal Vero cells. Mechanistic analysis revealed that treatment of the nanocomposite significantly enhanced intracellular reactive oxygen species (ROS) generation, disrupted mitochondrial membrane potential, and compromised plasma membrane integrity. Furthermore, the nanocomposite suppressed pro-inflammatory mediators (TNF-α, NF-κB, COX-2, and IL-6) and induced apoptosis, evidenced by elevated Bax, caspase-3, and caspase-9 levels alongside reduced Bcl-2 expression. Crucially, the formulated nanocomposite attenuated the PI3K/Akt/mTOR signaling pathway, a key regulator of bladder cancer progression. Despite these potent anti-oncogenic effects, challenges remain regarding the precise control of crocin release kinetics and the long-term metabolic clearance of the metallic zinc component. Future prospects involve validating these findings in orthotopic animal models to assess systemic toxicity and optimizing the formulation for targeted intravesical delivery to improve clinical translation.