Evaluation of Apoptotic Gene Expression in Hepatoma Cell Line (HepG2) Following Nisin Treatment

Nahid Zainodini1, Mohammad Reza Hajizadeh2,3, Mohammad Reza Mirzaei2,3

  • 1Immunology of Infectious Diseases Research Center, Research Institute of Basic Medical Sciences, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.

Abstract

Insights

Nisin effectively reduces hepatoma cell viability and induces apoptosis in HepG2 cells. This occurs through the activation of intrinsic apoptosis pathways, involving key genes like caspase-9 and BID.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Pharmacology

Background:

  • Hepatoma, specifically hepatocellular carcinoma, remains a significant global health concern.
  • Nisin, a bacteriocin, has demonstrated potential anti-cancer properties in preliminary studies.
  • Understanding nisin's mechanism of action in cancer cells is crucial for therapeutic development.

Purpose of the Study:

  • To evaluate the impact of nisin on the survival of the HepG2 hepatoma cell line.
  • To investigate nisin-induced apoptosis and identify the specific molecular pathways involved.

Main Methods:

  • Cell viability was assessed using the MTT assay following nisin treatment.
  • Apoptosis induction was quantified via Annexin-V/propidium iodide (PI) double staining.
  • The human apoptosis PCR array was employed to identify activated apoptosis-related genes and pathways.

Main Results:

  • Nisin significantly decreased HepG2 cell viability in a dose-dependent manner, with an IC50 of approximately 40 µg/ml.
  • Nisin treatment demonstrably induced apoptosis in HepG2 cells.
  • PCR array analysis revealed a notable upregulation of genes within the caspase and BCL2 families, crucial for apoptosis.

Conclusions:

  • Nisin induces apoptosis in HepG2 cells primarily through the intrinsic apoptosis pathway.
  • Upregulation of specific genes, including caspase-9 and BID, was observed, correlating with increased apoptosis.
  • These findings suggest nisin's potential as an anti-cancer agent targeting hepatoma cells.

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