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Eupatorin-induced cell death in human leukemia cells is dependent on caspases and activates the mitogen-activated protein kinase pathway.

Abstract
Eupatorin is a naturally occurring flavone that inhibits cell proliferation in human tumor cells. Here we demonstrate that eupatorin arrests cells at the G2-M phase of the cell cycle and induces apoptotic cell death involving activation of multiple caspases, mitochondrial release of cytochrome c and poly(ADP-ribose) polymerase cleavage in human leukemia cells. This flavonoid induced the phosphorylation of members of the mitogen-activated protein kinases and cell death was attenuated by inhibition of c-jun N-terminal kinases/stress activated protein kinases. Eupatorin-induced cell death is mediated by both the extrinsic and the intrinsic apoptotic pathways and through a mechanism dependent on reactive oxygen species generation.
AuthorsSara Estévez, María Teresa Marrero, José Quintana, Francisco Estévez
JournalPloS one (PLoS One) Vol. 9 Issue 11 Pg. e112536 ( 2014) ISSN: 1932-6203 [Electronic] United States
PMID25390937 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Antineoplastic Agents, Phytogenic
  • Flavonoids
  • Reactive Oxygen Species
  • eupatorin
  • Cytochromes c
  • Poly(ADP-ribose) Polymerases
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinases
  • Caspases
Topics
  • Antineoplastic Agents, Phytogenic (pharmacology)
  • Apoptosis (drug effects)
  • Caspases (genetics, metabolism)
  • Cell Division (drug effects)
  • Cell Line, Tumor
  • Cell Proliferation (drug effects)
  • Cytochromes c (metabolism)
  • Flavonoids (pharmacology)
  • G2 Phase Cell Cycle Checkpoints (drug effects)
  • Gene Expression Regulation, Neoplastic
  • HL-60 Cells
  • Humans
  • JNK Mitogen-Activated Protein Kinases (antagonists & inhibitors, genetics, metabolism)
  • Mitogen-Activated Protein Kinases (genetics, metabolism)
  • Phosphorylation (drug effects)
  • Poly(ADP-ribose) Polymerases (genetics, metabolism)
  • Proteolysis (drug effects)
  • Reactive Oxygen Species (metabolism)
  • Signal Transduction

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