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Evidence-Based Complementary and Alternative Medicine
Volume 2012 (2012), Article ID 580736, 11 pages
http://dx.doi.org/10.1155/2012/580736
Research Article

Retinoic Acid Induces Apoptosis of Prostate Cancer DU145 Cells through Cdk5 Overactivation

1Department of Life Sciences, National Chung Hsing University, Taichung 40227, Taiwan
2Department of Health and Nutrition Biotechnology, Asia University, Taichung 41354, Taiwan
3Graduate Institute of Basic Medical Science, China Medical University, Taichung 40402, Taiwan
4Department of Education and Research, Taichung Veterans General Hospital, Taichung 40705, Taiwan
5Department of Urology, Chang Bing Show Chwan Memorial Hospital, Changhua 50544, Taiwan
6Agricultural Biotechnology Center, National Chung Hsing University, Taichung 40227, Taiwan
7Graduate Institute of Rehabilitation Science, China Medical University, Taichung 40402, Taiwan
8Department of Urology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA

Received 21 August 2012; Revised 9 November 2012; Accepted 16 November 2012

Academic Editor: Chun-Tao Che

Copyright © 2012 Mei-Chih Chen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Supplementary Material

Supplementary Figure 1: RA triggered p25 formation and caspase-3 activation in prostate PC3 cancer cells. PC3 cells were treated as follows: control, RA (10 μM), RA+CP, CP (10 μM) for 4 days after 1-day serum-free pretreatment. Cleaved caspase-3 and p25 were detected by immunoblotting with specific antibodies as described in Materials and Methods. β-actin served as an internal control.

Supplementary Figure 2: The comparison of effects of all-trans-retinoic acid, 9-cis-retinoic acid, and 13-cis-retinoic acid on p25 formation and caspase-3 activation in prostate DU145 cancer cells. DU145 cells were treated as follows: control, all-trans-retinoic acid (10 μM), 9-cis-retinoic acid (10 μM), or 13-cis-retinoic acid (10 μM) for 4 days after 1-day serum-free pretreatment. Cleaved caspase-3 and p25 were detected by immunoblotting with specific antibodies as described in Materials and Methods. β-actin served as an internal control.

Supplementary Figure 3: RA-triggered p25 formation and caspase-3 activation can be diminished by calcium chelator, EGTA, in DU145 cells. DU145 cells were treated as follows: control, RA (10 μM), RA+EGTA, EGTA (0.5 mM) for 4 days after 1-day serum-free pretreatment. Cleaved caspase-3 and p25 were detected by immunoblotting with specific antibodies as described in Materials and Methods. β-actin served as an internal control.

  1. Supplementary Figures