6533b853fe1ef96bd12ad66e

RESEARCH PRODUCT

Cell cycle arrest and induction of apoptosis by cajanin stilbene acid from Cajanus cajan in breast cancer cells

Yuangang ZuMeng LuoYu-jie FuZuo-fu WeiBenjamin WienchChang GaoCheng-bo GuOnat KadiogluThomas Efferth

subject

Cell cycle checkpointDNA damageCellPharmaceutical ScienceApoptosisBiologyFlow cytometryCajanusStilbenesDrug DiscoverymedicineHumansbcl-2-Associated X ProteinMembrane Potential MitochondrialPharmacologymedicine.diagnostic_testCaspase 3Cell Cycle CheckpointsCell cycleMolecular biologySalicylatesGene Expression Regulation Neoplasticmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2Complementary and alternative medicineApoptosisCancer cellMCF-7 CellsMolecular MedicineDNA fragmentationDNA DamageSignal Transduction

description

Abstract Background: The low abundant cajanin stilbene acid (CSA) from Pigeon Pea ( Cajanus cajan ) has been shown to kill estrogen receptor α positive cancer cells in vitro and in vivo . Downstream effects such as cell cycle and apoptosis-related mechanisms have not been analyzed yet. Material and methods: We analyzed the activity of CSA by means of flow cytometry (cell cycle distribution, mitochondrial membrane potential, MMP), confocal laser scanning microscopy (MMP), DNA fragmentation assay (apoptosis), Western blotting (Bax and Bcl-2 expression, caspase-3 activation) as well as mRNA microarray hybridization and Ingenuity pathway analysis. Results: CSA induced G2/M arrest and apoptosis in a concentration-dependent manner from 8.88 to 14.79 µM. The MMP broke down, Bax was upregulated, Bcl-2 downregulated and caspase-3 activated. Microarray profiling revealed that CSA affected BRCA-related DNA damage response and cell cycle-regulated chromosomal replication pathways. Conclusion: CSA inhibited breast cancer cells by DNA damage and cell cycle-related signaling pathways leading to cell cycle arrest and apoptosis.

yearjournalcountryeditionlanguage
2015-04-01Phytomedicine
https://doi.org/10.1016/j.phymed.2015.02.005