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Chaetocin induces cell cycle arrest and apoptosis by regulating the ROS-mediated ASK-1/JNK signaling pathways

Jingliang He1, Xiaoxun Chen2, Bowei Li3

  • 1Department of General Surgery, Guangdong Second Provincial General Hospital, Guangzhou, Guangdong 510317, P.R. China.

Oncology Reports
|August 30, 2017
PubMed

Insights

Chaetocin, a natural compound, effectively reduced cholangiocarcinoma cell growth and invasion. It induces apoptosis by triggering oxidative stress and activating the ASK-1/JNK signaling pathway.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Cholangiocarcinoma (CCA) is a challenging cancer with limited treatment options.
  • Natural products are a promising source for novel anticancer agents.
  • Chaetocin, derived from Chaetomium fungi, shows potential anticancer properties.

Purpose of the Study:

  • To investigate the anticancer effects of chaetocin on human intrahepatic cholangiocarcinoma cells (CCLP-1).
  • To elucidate the molecular mechanisms underlying chaetocin-induced cell death.

Main Methods:

  • Cell viability and invasion assays (CCK-8, Transwell).
  • Flow cytometry and reactive oxygen species (ROS) assays.
  • Western blot analysis of apoptosis signaling pathways (ASK-1/JNK).
  • In vivo mouse xenograft tumor models.

Main Results:

  • Chaetocin significantly inhibited CCLP-1 cell viability and invasion in vitro and in vivo.
  • Chaetocin induced cell cycle arrest and apoptosis.
  • Chaetocin elevated intracellular ROS levels, causing oxidative stress.
  • Chaetocin upregulated the apoptosis signal-regulating kinase 1 (ASK-1) and c-Jun N-terminal kinase (JNK) signaling pathway.

Conclusions:

  • Chaetocin exhibits potent anticancer activity against intrahepatic cholangiocarcinoma.
  • The mechanism involves ROS-mediated activation of the ASK-1/JNK pathway, leading to cell cycle arrest and apoptosis.
  • Chaetocin represents a potential therapeutic candidate for cholangiocarcinoma treatment.

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