作者: Dongyue Liu , Anjun Liu
DOI: 10.1002/CBF.2912
关键词: Cell cycle 、 Cyclin E 、 Superoxide 、 Cell cycle checkpoint 、 Molecular biology 、 Superoxide dismutase 、 Cancer cell 、 Proliferating cell nuclear antigen 、 Biology 、 Cyclin-dependent kinase
摘要: As an efficient reactive oxygen species–scavenging enzyme, superoxide dismutase (SOD) has been shown to inhibit tumor growth and interfere with motility invasiveness of cancer cells. In this study, the molecular mechanisms cell cycle arrest when S180 cells were exposed high levels SOD investigated. Here, both murine sarcoma NIH-3T3 mouse fibroblasts respectively treated varying concentrations Cu/Zn-SOD for 24, 48 72 h determine optimal dose SOD, which was a concentration 800 U/ml h. It is found that induced at G1-phase decreasing level production, whereas had less effect on proliferation Moreover, expression rate Proliferating Cell Nuclear Antigen (PCNA) in suppressed after treatment, indicated inhibition DNA synthesis Besides, there significant down-regulations cyclin-E Cdk-2 contributed blockage G1/S transition cycle. Together, our data confirmed could notably induce by down-regulating expressions Cdk-2. Copyright © 2012 John Wiley & Sons, Ltd.