Activation of ROS-driven genomic instability, mitochondrial depolarization, and p53-independent apoptotic cell death in human A431 epidermoid skin cancer cells by bioactive glass nanoparticles - Report - MDSpire

Activation of ROS-driven genomic instability, mitochondrial depolarization, and p53-independent apoptotic cell death in human A431 epidermoid skin cancer cells by bioactive glass nanoparticles

  • By

  • Hanan R H Mohamed

  • Shahd Mosaad

  • Aya A. Osman

  • Alaa H. Elsewedy

  • Habiba M. Zaki

  • Mayada E. Borai

  • Gehan Safwat

  • April 2, 2026

  • 0 min

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Activation of ROS-driven genomic instability in A431 epidermoid skin cancer cells

Overview

This study investigates the effects of bioactive glass nanoparticles (BGNPs) on human A431 epidermoid skin cancer cells, revealing their potential to induce reactive oxygen species (ROS), genomic instability, and p53-independent apoptotic cell death. These findings suggest a novel therapeutic avenue for treating cutaneous squamous cell carcinoma (cSCC).

Background

Cutaneous squamous cell carcinoma (cSCC) is a prevalent form of skin cancer with rising incidence rates, particularly among high-risk populations. Current treatment options often fall short due to issues such as systemic toxicity and drug resistance. There is an urgent need for innovative therapies that can effectively target malignant cells while minimizing harm to healthy tissue.

Data Highlights

No numerical data or trial data was provided in the source material.

Key Findings

  • BGNPs induce ROS generation in A431 epidermoid skin cancer cells.
  • Exposure to BGNPs leads to genomic instability in these cancer cells.
  • Apoptotic cell death occurs independently of the p53 pathway when treated with BGNPs.
  • BGNPs exhibit selective cytotoxicity against cancer cells while sparing normal skin cells.
  • The study highlights the need for further research into the mechanisms of action of BGNPs in epithelial malignancies.

Clinical Implications

The findings suggest that BGNPs could serve as a promising therapeutic agent for cSCC, potentially improving treatment outcomes. Clinicians should consider the implications of ROS-driven mechanisms in cancer therapy and the development of targeted nanotechnology-based treatments.

Conclusion

The study underscores the potential of bioactive glass nanoparticles as a novel approach to treating epidermoid skin cancer, warranting further investigation into their therapeutic applications.

References

  1. Janostiak et al., Archives of Toxicology, 2019 -- The BH3 mimetic (±) gossypol triggers apoptosis and mitochondrial impairment in human A375 melanoma cells independent of ROS in vitro
  2. Boffetta et al., Archives of Toxicology, 2025 -- Co-exposure to Benzo[a]pyrene and UV Radiation: Varied Impacts on Oxidative Stress and Genotoxic Effects in Human Keratinocytes and Ex Vivo Skin
  3. Lee et al., Archives of Toxicology, 2018 -- Fine particulate matter 2.5 contributes to skin cell damage through oxidative stress, dysfunction of subcellular organelles, and induction of apoptosis
  4. Management of Regional Lymph Nodes in Clinically Node-Negative Cutaneous Squamous Cell Carcinoma of the Head and Neck: A Systematic Review & Meta-Analysis - PubMed
  5. A phase 2 open-label study of cemiplimab in patients with advanced cutaneous squamous cell carcinoma (EMPOWER-CSCC-1): Final long-term analysis of groups 1, 2, and 3, and primary analysis of fixed-dose treatment group 6 - ScienceDirect
  6. Archives of Toxicology — Gasdermin D-formed membrane pores regulate the release of IL-1α from necrotic macrophages following exposure to silica rich in NFS
  7. Genomic Insights into Cutaneous Squamous Cell Carcinoma - PMC
  8. Management of Regional Lymph Nodes in Clinically Node-Negative Cutaneous Squamous Cell Carcinoma of the Head and Neck: A Systematic Review & Meta-Analysis - PubMed
  9. A phase 2 open-label study of cemiplimab in patients with advanced cutaneous squamous cell carcinoma (EMPOWER-CSCC-1): Final long-term analysis of groups 1, 2, and 3, and primary analysis of fixed-dose treatment group 6 - ScienceDirect

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