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

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.
AuthorsZhiwei Quan, Jun Gu, Ping Dong, Jianhua Lu, Xiangsong Wu, Wenguang Wu, Xiaozhou Fei, Songgang Li, Yong Wang, Jianwei Wang, Yingbin Liu
JournalCancer letters (Cancer Lett) Vol. 295 Issue 2 Pg. 252-9 (Sep 28 2010) ISSN: 1872-7980 [Electronic] Ireland
PMID20359814 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Copyright2010 Elsevier Ireland Ltd. All rights reserved.
Chemical References
  • Antineoplastic Agents, Phytogenic
  • DDIT3 protein, human
  • Flavones
  • Reactive Oxygen Species
  • Transcription Factor CHOP
  • cirsimaritin
  • Cytochromes c
  • Proto-Oncogene Proteins c-akt
  • Caspases
Topics
  • Antineoplastic Agents, Phytogenic (pharmacology)
  • Apoptosis (drug effects)
  • Caspases (metabolism)
  • Cell Line, Tumor
  • Cytochromes c (metabolism)
  • Endoplasmic Reticulum (drug effects, metabolism)
  • Flavones (pharmacology)
  • Gallbladder Neoplasms (drug therapy, pathology)
  • Humans
  • Membrane Potential, Mitochondrial (drug effects)
  • Mitochondria (physiology)
  • Proto-Oncogene Proteins c-akt (physiology)
  • Reactive Oxygen Species (metabolism)
  • Transcription Factor CHOP (physiology)

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