Published online Apr 21, 2015. doi: 10.3748/wjg.v21.i15.4526
Peer-review started: September 14, 2014
First decision: October 14, 2014
Revised: November 11, 2014
Accepted: January 8, 2015
Article in press: January 8, 2015
Published online: April 21, 2015
Processing time: 222 Days and 6 Hours
AIM: To investigate the effect of alternol on pancreatic cancer cells.
METHODS: Pancreatic cancer cells PANC-1 and BxPC3 were treated with various concentrations of alternol for 24, 48 and 72 h. Cell proliferation was measured by cell counting. Cell cycle distribution and mitochondrial membrane potential were determined by flow cytometry. Apoptosis was determined by a TdT-mediated dUTP nick end labeling assay and Hoechst staining. Expression of caspase 3, Bcl-2, p53 and p21 was measured by western blotting.
RESULTS: Alternol showed dose- and time-dependent inhibition of the proliferation of PANC-1 and BxPC3 cells in vitro. Alternol induced apoptosis and cell cycle arrest at S phase and decreased mitochondrial membrane potential. Alternol activated caspase 3, upregulated p53 and p21 expression, and downregulated Bcl-2 expression in a dose-dependent manner.
CONCLUSION: Our results suggested that alternol is a candidate for treatment of pancreatic cancer.
Core tip: Pancreatic cancer is an aggressive disease with a 5-year survival < 5%. Alternol has shown anti-cancer activity against various types of cancer cells. The aim of this study was to investigate the effect of alternol on pancreatic cancer cells. Alternol inhibited proliferation of PANC-1 and BxPC3 cells. It induced apoptosis and cell cycle arrest and decreased mitochondrial membrane potential. Alternol activated caspase 3, upregulated p53 and p21 expression, and downregulated Bcl-2 expression. In summary, we concluded that alternol may provide an effective regimen for the treatment of pancreatic cancer.