Nisin induces apoptosis in cervical cancer cells via reactive oxygen species generation and mitochondrial membrane

Houri Sadri1, Mahmoud Aghaei2,3, Vajihe Akbari1,3

  • 1Department of Pharmaceutical Biotechnology, Faculty of Pharmacy, Isfahan University of Medical Sciences, Isfahan, Iran.

Insights

Nisin, an antimicrobial peptide, shows potential as an anticancer agent by inducing cell death in cervical cancer cells. It selectively targets cancer cells, offering a promising therapeutic avenue with minimal toxicity to normal cells.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Pharmacology

Background:

  • Nisin is a food-grade antimicrobial peptide with emerging anticancer properties.
  • Understanding nisin's mechanism against cancer is crucial for therapeutic development.

Purpose of the Study:

  • To evaluate nisin's cytotoxicity and apoptotic effects on human cancer cell lines.
  • To investigate the role of mitochondrial dysfunction and oxidative stress in nisin-induced apoptosis.

Main Methods:

  • Cytotoxicity assessed via MTT assay in HeLa, OVCAR-3, SK-OV-3, and HUVEC cell lines.
  • Apoptosis confirmed using Annexin-V/propidium iodide staining, western blotting, mitochondrial membrane potential (ΔΨm) analysis, and reactive oxygen species (ROS) assays.

Main Results:

  • Nisin exhibited concentration-dependent cytotoxicity against cancer cells (IC50: 11.5–23 µM) with lower toxicity to normal HUVECs.
  • Nisin treatment (12 µM) significantly increased the Bax/Bcl-2 ratio (4.9-fold), decreased ΔΨm (70%), and elevated ROS levels (1.7-fold) in cervical cancer cells.
  • These changes suggest nisin induces apoptosis via mitochondrial dysfunction and oxidative stress.

Conclusions:

  • Nisin demonstrates significant anticancer and apoptogenic activities against cervical cancer cells.
  • The mechanism involves inducing mitochondrial dysfunction and oxidative stress, leading to apoptosis.
  • Nisin presents a potential therapeutic candidate for cervical cancer treatment.

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