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Evaluating Cell Death Using Cell-Free Supernatant of Probiotics in Three-Dimensional Spheroid Cultures of Colorectal Cancer Cells
06:07

Evaluating Cell Death Using Cell-Free Supernatant of Probiotics in Three-Dimensional Spheroid Cultures of Colorectal Cancer Cells

Published on: June 13, 2020

Activation of several concurrent proapoptic pathways by sulforaphane in human colon cancer cells SW620

E Rudolf1, H Andelová, M Cervinka

  • 1Department of Medical Biology and Genetics, Charles University in Prague, Faculty of Medicine in Hradec Kralove, Simkova 870, Hradec Kralove, Czech Republic. rudolf@lfhk.cuni.cz

Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association
|July 1, 2009
PubMed

Insights

Sulforaphane (SF) triggers apoptosis in colon cancer cells via DNA-damage and caspase-2-JNK pathways. These mechanisms, independent of ROS, highlight SF

Area of Science:

  • * Oncology
  • * Molecular Biology
  • * Cancer Research

Background:

  • * Sulforaphane (SF) exhibits known cytotoxicity and apoptosis-inducing effects in colon cancer cells.
  • * The precise molecular mechanisms and signaling pathways of SF-mediated apoptosis remain incompletely understood.
  • * Investigating these pathways is crucial for understanding SF's potential as a chemopreventive agent.

Purpose of the Study:

  • * To elucidate the specific mechanisms and signaling cascades of SF-induced apoptosis in advanced colon cancer.
  • * To investigate SF's effects on proapoptotic signaling in the metastatic SW620 cell line.
  • * To determine the role of p53 status and mitochondrial activity in SF's apoptotic effects.

Main Methods:

  • * Utilized the metastatic SW620 colon cancer cell line for experimental analysis.
  • * Investigated the DNA-damage response pathway and its interaction with p53.
  • * Examined the caspase-2-JNK pathway and its dependence on p53 status and mitochondrial activity.
  • * Assessed the involvement of reactive oxygen species (ROS) in SF-induced apoptosis.

Main Results:

  • * SF induces multivariate apoptotic cascades in SW620 cells.
  • * Proapoptotic signaling via the DNA-damage response pathway is attenuated by mutant p53.
  • * The caspase-2-JNK pathway complements p53-dependent signaling in wild-type p53 cells.
  • * Both investigated pathways necessitate active mitochondria and do not rely on ROS generation.

Conclusions:

  • * SF activates distinct apoptotic signaling pathways in colon cancer cells, influenced by p53 status.
  • * Mitochondrial activity is essential for SF-induced apoptosis, independent of ROS.
  • * SF demonstrates potential as a chemopreventive agent against colon cancer, warranting further investigation.

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