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Trabectedin (ET-743) in prostate cancer: Endoplasmic reticulum stress-induced apoptotic effect

Harika Atmaca1, Ferdi Oğuz2, Suleyman Ilhan1

  • 1Department of Biology, Faculty of Science and Letters, Manisa Celal Bayar University, Manisa, Turkey.

Andrologia
|September 28, 2022
PubMed

Insights

Trabectedin shows potential as a prostate cancer (PCa) treatment by inducing cell death and halting cell cycle progression. It functions independently of DNA, triggering endoplasmic reticulum stress and apoptosis in PCa cells.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Prostate cancer (PCa) remains a significant health concern, necessitating novel therapeutic strategies.
  • Trabectedin, a marine-derived chemotherapy agent, has shown efficacy in various cancers.
  • Its DNA-independent mechanisms in PCa are not fully elucidated.

Purpose of the Study:

  • To investigate the DNA-independent mechanisms of trabectedin in prostate cancer (PCa) cells.
  • To evaluate trabectedin's effects on cell viability, apoptosis, mitochondrial membrane potential (MMP), cell cycle, reactive oxygen species (ROS) generation, and endoplasmic reticulum (ER) stress.
  • To determine the potential of trabectedin as a chemotherapeutic agent for PCa.

Main Methods:

  • Cell viability assessed using XTT assay.
  • Apoptosis and cell cycle distribution analyzed via flow cytometry.
  • Mitochondrial membrane potential (MMP) measured using TMRE dye.
  • Reactive oxygen species (ROS) monitored with CM-H2DCFDA dye.
  • Western blot analysis performed for ER stress markers (CHOP, p-eIF2α, GRP78, p-PERK).

Main Results:

  • Trabectedin induced significant cytotoxicity and cell cycle arrest at the G2/M phase in PCa cells.
  • The drug decreased MMP through ROS generation.
  • Elevated levels of ER stress proteins (CHOP, p-eIF2α, GRP78, p-PERK) indicated ER stress-induced apoptosis.
  • These effects occurred independently of DNA interaction.

Conclusions:

  • Trabectedin effectively induces apoptosis and cell cycle arrest in PCa cells through ROS generation and ER stress.
  • The study supports trabectedin's potential as a novel chemotherapeutic agent for prostate cancer.
  • Understanding these DNA-independent mechanisms could lead to optimized therapeutic applications.
Keywords:
ER stressapoptosiscytotoxicityoxidative stressprostate cancertrabectedin

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