Reactive oxygen species-mediated endoplasmic reticulum stress and mitochondrial dysfunction contribute to cirsimaritin-induced apoptosis in human gallbladder carcinoma GBC-SD cells

Cancer Lett. 2010 Sep 28;295(2):252-9. doi: 10.1016/j.canlet.2010.03.008. Epub 2010 Mar 31.

Abstract

In this study, the anticancer effect of cirsimaritin, a natural flavonoid, against human gallbladder carcinoma cell line GBC-SD and the underlying mechanisms were investigated. Cirsimaritin inhibited the growth of tumor cells and induced mitochondrial apoptosis in GBC-SD cells. In addition, cirsimaritin triggered endoplasmic reticulum (ER) stress and down-regulated the phosphorylation of Akt, while knock-down of CHOP dramatically abrogated the inactivation of Akt and reversed the pro-apoptotic effect of cirsimaritin. Furthermore, cirsimaritin provoked the generation of reactive oxygen species in GBC-SD cells, while the antioxidant N-acetyl cysteine almost completely blocked the activation of ER stress and apoptosis, suggesting cirsimaritin-induced reactive oxygen species is an early event that triggers ER stress mitochondrial apoptotic pathways in GBC-SD cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents, Phytogenic / pharmacology*
  • Apoptosis / drug effects*
  • Caspases / metabolism
  • Cell Line, Tumor
  • Cytochromes c / metabolism
  • Endoplasmic Reticulum / drug effects*
  • Endoplasmic Reticulum / metabolism
  • Flavones / pharmacology*
  • Gallbladder Neoplasms / drug therapy*
  • Gallbladder Neoplasms / pathology
  • Humans
  • Membrane Potential, Mitochondrial / drug effects
  • Mitochondria / physiology*
  • Proto-Oncogene Proteins c-akt / physiology
  • Reactive Oxygen Species / metabolism*
  • Transcription Factor CHOP / physiology

Substances

  • Antineoplastic Agents, Phytogenic
  • DDIT3 protein, human
  • Flavones
  • Reactive Oxygen Species
  • Transcription Factor CHOP
  • cirsimaritin
  • Cytochromes c
  • Proto-Oncogene Proteins c-akt
  • Caspases