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Didymin induces apoptosis through mitochondrial dysfunction and up-regulation of RKIP in human hepatoma cells

Jinbin Wei1, Quanfang Huang2, Facheng Bai1

  • 1Guangxi Medical University, Nanning 530021, China.

Chemico-Biological Interactions
|December 1, 2016
PubMed

Insights

Origanum vulgare didymin (OVD) effectively inhibits liver cancer cell growth and migration. This flavonoid induces apoptosis and cell cycle arrest by impacting key molecular pathways and mitochondrial function.

Area of Science:

  • Phytochemistry
  • Molecular Biology
  • Cancer Research

Background:

  • Hepatocellular carcinoma (HCC) remains a significant global health challenge.
  • Natural compounds offer potential therapeutic avenues for cancer treatment.
  • Origanum vulgare is a medicinal herb with known bioactive constituents.

Purpose of the Study:

  • To investigate the anti-cancer effects of didymin isolated from Origanum vulgare (OVD) on human HepG2 liver carcinoma cells.
  • To elucidate the underlying molecular mechanisms of OVD-induced anti-cancer activity.

Main Methods:

  • Isolation and identification of didymin from Origanum vulgare.
  • Assessment of OVD's effects on HepG2 cell viability, clonogenicity, and migration.
  • Analysis of cell cycle progression and apoptosis induction.
  • Evaluation of mitochondrial membrane potential and cytochrome c release.
  • Investigation of signaling pathways, including ERK/MAPK, PI3K/Akt, and RKIP levels.

Main Results:

  • OVD significantly inhibited HepG2 cell viability, clonogenicity, and migration.
  • OVD induced G2/M phase cell cycle arrest by regulating cyclin B1, cyclin D1, and CDK4.
  • OVD promoted apoptosis via modulation of the Bcl-2/Bax ratio and caspase activation.
  • OVD attenuated mitochondrial membrane potential and induced cytochrome c release.
  • OVD inhibited ERK/MAPK and PI3K/Akt pathways by up-regulating RKIP.

Conclusions:

  • Origanum vulgare didymin (OVD) exhibits potent anti-cancer properties against HepG2 liver carcinoma cells.
  • OVD induces apoptosis and cell cycle arrest through mitochondrial dysfunction and inactivation of key signaling pathways.
  • Up-regulation of RKIP by OVD plays a crucial role in inhibiting ERK/MAPK and PI3K/Akt pathways.
Keywords:
DidyminERK/MAPK pathwayMitochondrial dysfunctionPI3K/Akt pathwayRKIP

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