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Melatonin Induces Autophagy via Reactive Oxygen Species-Mediated Endoplasmic Reticulum Stress Pathway in Colorectal

Kian Chung Chok1, Rhun Yian Koh2, Ming Guan Ng1

  • 1School of Health Science, International Medical University, Kuala Lumpur 57000, Malaysia.

Molecules (Basel, Switzerland)
|August 27, 2021
PubMed

Insights

Melatonin, a natural compound, triggers cell death and autophagy in colorectal cancer (CRC) cells. This study reveals melatonin

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Colorectal cancer (CRC) remains a significant cause of cancer mortality despite advances in treatment.
  • Melatonin exhibits known anticancer properties, including anti-inflammatory and pro-apoptotic effects.
  • The precise mechanisms of melatonin's action in CRC, particularly involving autophagy, require further elucidation.

Purpose of the Study:

  • To investigate the role of autophagy pathways in colorectal cancer (CRC) cells treated with melatonin.
  • To explore how melatonin influences cell death and oxidative stress in CRC models.
  • To identify specific signaling pathways modulated by melatonin in CRC.

Main Methods:

  • In vitro treatment of CRC cell lines (HT-29, SW48, Caco-2) with melatonin.
  • Assessment of cell death, oxidative stress, and autophagic vacuole formation.
  • Examination of key autophagy-related signaling pathways: endoplasmic reticulum (ER) stress, AMPK, PI3K, Akt, and mTOR.

Main Results:

  • Melatonin induced CRC cell death, oxidative stress, and autophagic vacuole formation in a dose-dependent manner.
  • Melatonin significantly activated autophagy.
  • The endoplasmic reticulum (ER) stress pathway was identified as a key mediator of melatonin-induced autophagy in CRC cells.

Conclusions:

  • Melatonin effectively induces autophagy in colorectal cancer cells, primarily through the ER stress pathway.
  • Melatonin demonstrates significant potential as an anticancer therapeutic agent for colorectal cancer.
  • Further research into melatonin's mechanisms could lead to novel CRC treatment strategies.
Keywords:
autophagycolorectal cancer cellsendoplasmic reticulum stressmelatoninreactive oxygen species

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