Jungim Kim1, Atsushi Mizokami2, Minkyoung Shin1, Kouji Izumi1, Hiroyuki Konaka1, Yoshifumi Kadono1, Yasuhide Kitagawa1, Evan T Keller3, Jian Zhang4, Mikio Namiki1. 1. Department of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, Japan. 2. Department of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, Japan mizokami@med.kanazawa-u.ac.jp. 3. Department of Urology and Pathology, University of Michigan, Ann Arbor, MI, U.S.A. 4. Center for Translational Medicine, Guangxi Medical University, Nanning, Guangxi, China.
Abstract
BACKGROUND: The functions of superoxide dismutase-3 (SOD3), which acts on the cell surface and protects cells from oxidative stress, remain uncertain in the progression of prostate cancer. MATERIALS AND METHODS: To verify SOD3 expression in human prostate tissue, immunohistochemistry was performed using tissue microarrays. To investigate the effects of SOD3 on proliferation, migration, and invasion, SOD3 was overexpressed and recombinant SOD3 was employed in PC-3 prostate cancer cells. H2O2 levels, reduced glutathione (GSH)/oxidized glutathione (GSSG) ratio, catalase activity, and 8-oxo-2'-deoxyguanosine (8-OHdG) were estimated in SOD3-overexpressing PC-3 cells. RESULTS: Immunohistochemistry revealed reduced expression of SOD3 in prostate cancer tissue. SOD3 overexpression in PC-3 cells inhibited cell proliferation, migration, and invasion. Recombinant SOD3 had the same effect. H2O2 accumulation was increased by SOD3 overexpression, GSH/GSSG ratio was decreased, and catalase activity was decreased. DNA damage in SOD3-overexpressing cells was confirmed by 8-OHdG elevation. CONCLUSION: Since SOD3 acts as a tumor suppressor, SOD3 overexpression and recombinant SOD3 might lead to treatment for prostate cancer. Copyright
BACKGROUND: The functions of superoxide dismutase-3 (SOD3), which acts on the cell surface and protects cells from oxidative stress, remain uncertain in the progression of prostate cancer. MATERIALS AND METHODS: To verify SOD3 expression in human prostate tissue, immunohistochemistry was performed using tissue microarrays. To investigate the effects of SOD3 on proliferation, migration, and invasion, SOD3 was overexpressed and recombinant SOD3 was employed in PC-3 prostate cancer cells. H2O2 levels, reduced glutathione (GSH)/oxidized glutathione (GSSG) ratio, catalase activity, and 8-oxo-2'-deoxyguanosine (8-OHdG) were estimated in SOD3-overexpressing PC-3 cells. RESULTS: Immunohistochemistry revealed reduced expression of SOD3 in prostate cancer tissue. SOD3 overexpression in PC-3 cells inhibited cell proliferation, migration, and invasion. Recombinant SOD3 had the same effect. H2O2 accumulation was increased by SOD3 overexpression, GSH/GSSG ratio was decreased, and catalase activity was decreased. DNA damage in SOD3-overexpressing cells was confirmed by 8-OHdG elevation. CONCLUSION: Since SOD3 acts as a tumor suppressor, SOD3 overexpression and recombinant SOD3 might lead to treatment for prostate cancer. Copyright
Authors: Tobias Nordström; Erin L Van Blarigan; Vy Ngo; Ritu Roy; Vivian Weinberg; Xiaoling Song; Jeffry Simko; Peter R Carroll; June M Chan; Pamela L Paris Journal: Prostate Date: 2015-11-20 Impact factor: 4.104
Authors: Philippe Collery; Ahmed Mohsen; Anthony Kermagoret; Samantha Corre; Gérard Bastian; Alain Tomas; Ming Wei; François Santoni; Nadia Guerra; Didier Desmaële; Jean d'Angelo Journal: Invest New Drugs Date: 2015-06-26 Impact factor: 3.850