Abstract
Manganese superoxide dismutase (Mn-SOD), localized at the mitochondrial matrix, has the ability to protect cells against oxidative damage. It has been reported that low levels of Mn-SOD gene expression cause the development of certain kind of tumors. On the other hand, overexpression of Mn-SOD gene may play an important role in the development of cancer. In our study, we find that Mn-SOD activity was higher in nonaggressive (MCF-7) and aggressive (BT-549 and 11-9-14) breast cancer cell lines compared to that of nontumorigenic (MCF-12A and MCF-12F) mammary epithelial cell lines. We also observed an increased expression of Mn-SOD gene in cancerous cell lines. The elevated level of SOD activity in nonaggressive and aggressive breast epithelial cell lines was associated with some changes in nucleotide sequence.
Highlights
IntroductionThe third most common cancer worldwide, accounts for the highest morbidity and mortality [1]
Carcinoma of the breast, the third most common cancer worldwide, accounts for the highest morbidity and mortality [1]
We find that Manganese superoxide dismutase (Mn-Superoxide dismutase (SOD)) activity was higher in nonaggressive (MCF-7) and aggressive (BT-549 and 11-9-14) breast cancer cell lines compared to that of nontumorigenic (MCF-12A and MCF-12F) mammary epithelial cell lines
Summary
The third most common cancer worldwide, accounts for the highest morbidity and mortality [1]. It is the second leading cause of cancer death in women, after lung cancer [2]. Reactive oxygen species (ROS), such as superoxide anions and hydrogen peroxideinduced lipid peroxidation, play a major role in malignant transformation [4] and tumor cell proliferation and invasion [5, 6, 7]. It has been hypothesized that the production of ROS in combination with a decrease in the activity of antioxidant enzymes may be characteristic of tumor cells [8, 9]
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.