Basic Research
Copyright ©The Author(s) 2004. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jan 1, 2004; 10(1): 105-111
Published online Jan 1, 2004. doi: 10.3748/wjg.v10.i1.105
Red oil A5 inhibits proliferation and induces apoptosis in pancreatic cancer cells
Mi-Lian Dong, Xian-Zhong Ding, Thomas E. Adrian
Mi-Lian Dong, Affiliated Taizhou Hospital, Wenzhou Medical College, Linhai 317000, Zhejiang Province, China
Xian-Zhong Ding, Thomas E. Adrian, Northwestern University Medical School, Chicago, IL60611-3008, USA
Author contributions: All authors contributed equally to the work.
Supported by the National Cancer Institute of USA, No. CA72712, and Special Funds for Zhejiang 151 Talent Project of China, No. 98-2095
Correspondence to: Mi-Lian Dong, Taizhou Hospital of Wenzhou Medical College, 150 Ximen Street, Linhai 317000, Zhejiang Province, China. mdong2@hotmail.com
Telephone: +86-576-5315829 Fax: +86-576-5315829
Received: June 4, 2003
Revised: July 20, 2003
Accepted: August 16, 2003
Published online: January 1, 2004
Abstract

AIM: To study the effect of red oil A5 on pancreatic cancer cells and its possible mechanisms.

METHODS: Effect of different concentrations of red oil A5 on proliferation of three pancreatic cancer cell lines, AsPC-1, MiaPaCa-2 and S2013, was measured by 3H-methyl thymidine incorporation. Time-dependent effects of 1:32 000 red oil A5 on proliferation of three pancreatic cancer cell lines, were also measured by 3H-methyl thymidine incorporation, and Time-course effects of 1:32 000 red oil A5 on cell number. The cells were counted by Z1-Coulter Counter. Flow-cytometric analysis of cellular DNA content in the control and red oil A5 treated AsPC-1, MiaPaCa-2 and S2013 cells, were stained with propidium iodide. TUNEL assay of red oil A5-induced pancreatic cancer cell apoptosis was performed. Western blotting of the cytochrome c protein in AsPC-1, MiaPaCa-2 and S2013 cells treated 24 hours with 1:32 000 red oil A5 was performed. Proteins in cytosolic fraction and in mitochondria fraction were extracted. Proteins extracted from each sample were electrophoresed on SDS-PAGE gels and then were transferred to nitrocellulose membranes. Cytochrome c was identified using a monoclonal cytochrome c antibody. Western blotting of the caspase-3 protein in AsPC-1, MiaPaCa-2 and S2013 cells treated with 1:32 000 red oil A5 for 24 hours was carried out. Proteins in whole cellular lysates were electrophoresed on SDS-PAGE gels and then transferred to nitrocellulose membranes. Caspase-3 was identified using a specific antibody. Western blotting of poly-ADP ribose polymerase (PARP) protein in AsPC-1, MiaPaCa-2 and S2013 cells treated with 1:32 000 red oil A5 for 24 hours was performed. Proteins in whole cellular lysates were separated by electrophoresis on SDS-PAGE gels and then transferred to nitrocellulose membranes. PARP was identified by using a monoclonal antibody.

RESULTS: Red oil A5 caused dose- and time-dependent inhibition of pancreatic cancer cell proliferation. Propidium iodide DNA staining showed an increase of the sub-G0/G1 cell population. The DNA fragmentation induced by red oil A5 in these three cell lines was confirmed by the TUNEL assay. Furthermore, Western blotting analysis indicated that cytochrome c was released from mitochondria to cytosol during apoptosis, and caspase-3 was activated following red oil A5 treatment which was measured by procaspase-3 cleavage and PARP cleavage.

CONCLUSION: These findings show that red oil A5 has potent anti-proliferative effects on human pancreatic cancer cells with induction of apoptosis in vitro.

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