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Melatonin induces apoptosis in cholangiocarcinoma cell lines by activating the reactive oxygen species-mediated

Umawadee Laothong1, Yusuke Hiraku2, Shinji Oikawa2

  • 1Department of Parasitology, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand.

Oncology Reports
|January 22, 2015
PubMed

Insights

Melatonin, a natural compound, effectively reduces cholangiocarcinoma (CCA) cell viability. It induces cell death by increasing reactive oxygen species (ROS), DNA damage, and apoptosis in CCA cells.

Area of Science:

  • Oncology
  • Biochemistry
  • Molecular Biology

Background:

  • Melatonin's chemopreventive potential against cholangiocarcinoma (CCA) was previously shown in a hamster model.
  • The precise cytotoxic mechanisms of melatonin in cancer cells require further elucidation.

Purpose of the Study:

  • To investigate the cytotoxic effects of melatonin on human cholangiocarcinoma (CCA) cell lines.
  • To determine the underlying molecular mechanisms of melatonin-induced CCA cell death.

Main Methods:

  • Human CCA cell lines (KKU-M055 and KKU-M214) were treated with varying concentrations of melatonin (0.5, 1, and 2 mM) for 48 hours.
  • Assessed cell viability, intracellular reactive oxygen species (ROS) production, oxidative DNA damage (8-oxodG formation), and apoptosis-related protein expression (cytochrome c, caspase-3, caspase-7).

Main Results:

  • Melatonin exhibited a concentration-dependent inhibition of CCA cell viability.
  • Melatonin treatment increased intracellular ROS production, leading to heightened oxidative DNA damage and 8-oxodG formation.
  • Melatonin enhanced cytochrome c production and the expression of apoptosis-related proteins (caspase-3 and caspase-7), indicating induced apoptosis.

Conclusions:

  • Melatonin acts as a pro-oxidant in CCA cells.
  • Melatonin induces apoptosis in CCA cells through ROS-dependent DNA damage and activation of the apoptotic pathway.

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