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Farnesol induces apoptosis of DU145 prostate cancer cells through the PI3K/Akt and MAPK pathways.

Abstract
The aim of this study was to investigate the effect of farnesol on the induction of apoptosis in DU145 prostate cancer cells. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay showed that cell proliferation decreased significantly in a dose- and time-dependent manner. 4',6-Diamidino-2-phenylindole staining showed that chromatin condensation in cells treated with 60 µM of farnesol was markedly higher than in the control groups. Farnesol increased the expression of p53, p-c-Jun N-terminal kinase, cleaved-caspase-3, Bax, and cleaved-caspase-9, but decreased the expression of p-phosphatidylinositol-3-kinase (PI3K), p-Akt, p-p38, Bcl-2, and p-extracellular signal-regulated protein kinase, in a dose-dependent manner. The apoptotic cell ratio increased in a dose-dependent manner. The tumor growth inhibitory effect of farnesol was investigated in a mouse model. Compared to the control group, tumor volume decreased significantly in the group administered 50 mg/kg farnesol. Apoptosis was frequently detected in this same group by terminal deoxynucleotidyl transferase dUTP nick-end labeling assay. The results indicated that farnesol induced apoptosis of DU145 prostate cancer cells through the PI3K/Akt and mitogen-activated protein kinase signaling pathways.
AuthorsJin Soo Park, Jung Ki Kwon, Hye Ri Kim, Hyeong Jin Kim, Byeong Soo Kim, Ji Youn Jung
JournalInternational journal of molecular medicine (Int J Mol Med) Vol. 33 Issue 5 Pg. 1169-76 (May 2014) ISSN: 1791-244X [Electronic] Greece
PMID24584843 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Farnesol
  • Phosphatidylinositol 3-Kinase
  • Proto-Oncogene Proteins c-akt
  • Mitogen-Activated Protein Kinases
Topics
  • Apoptosis (drug effects)
  • Cell Line, Tumor
  • Farnesol (pharmacology)
  • Humans
  • Male
  • Mitogen-Activated Protein Kinases (metabolism)
  • Phosphatidylinositol 3-Kinase (metabolism)
  • Proto-Oncogene Proteins c-akt (metabolism)
  • Signal Transduction (drug effects)

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