scholarly journals Hop proanthocyanidins induce apoptosis, protein carbonylation, and cytoskeleton disorganization in human colorectal adenocarcinoma cells via reactive oxygen species

2009 ◽  
Vol 47 (4) ◽  
pp. 827-836 ◽  
Author(s):  
Woon-Gye Chung ◽  
Cristobal L. Miranda ◽  
Jan F. Stevens ◽  
Claudia S. Maier
Keyword(s):  
Reactive Oxygen Species ◽  
Colorectal Adenocarcinoma ◽  
Reactive Oxygen ◽  
Protein Carbonylation ◽  
Oxygen Species ◽  
Adenocarcinoma Cells ◽  
Apoptosis Protein

Superoxide dismutase mRNA and protein level in human colorectal cancer

2010 ◽  
Vol 5 (5) ◽  
pp. 590-599 ◽  
Author(s):  
Michał Skrzycki ◽  
Monika Majewska ◽  
Hanna Czeczot
Keyword(s):  
Colorectal Cancer ◽  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Liver Metastases ◽  
Tumor Cells ◽  
Protein Level ◽  
Colorectal Adenocarcinoma ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Colorectal Cancer Liver Metastases

AbstractImpairments of antioxidant enzyme expression are often concomitant with the onset of cancer. Due to epigenetic factors causing an inflammatory state the gastrointestinal tract can become exposed to reactive oxygen species. The purpose of our work was to evaluate mRNA and protein levels of superoxide dismutase isoenzymes in human colorectal adenocarcinoma due to its clinical advancement, and in colorectal cancer liver metastases. Evaluation of SOD expression in regard to CRC advancement, seems useful for clinical applications due to different tumor cells sensitivity to reactive oxygen species based treatment. Studies were conducted on a group of 27 patients: 15 diagnosed with colorectal adenocarcinoma and 12 diagnosed with colorectal cancer liver metastases. The mRNA level was determined by RT-PCR, and protein level by Western blotting. We observed significant (P≤0.05) changes of mRNA and protein level of SOD isoenzymes in subsequent stages of colorectal adenocarcinoma advancement and in colorectal cancer liver metastases. Differences in mRNA and protein level of SOD isoenzymes in colorectal adenocarcinoma and its liver metastases indicates that SOD participate in adaptation of tumor cells to oxidative stress, and maintain certain level of ROS, necessary for appropriate cell proliferation. Expression of superoxide dismutase isoenzymes seems to be regulated not only at transcriptional level, but also posttranscriptional.

scholarly journals Sanguinarine Inhibits Vascular Endothelial Growth Factor Release by Generation of Reactive Oxygen Species in MCF-7 Human Mammary Adenocarcinoma Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Xian-zhe Dong ◽  
Miao Zhang ◽  
Kun Wang ◽  
Ping Liu ◽  
Dai-hong Guo ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Mammary Adenocarcinoma ◽  
Vascular Endothelial ◽  
Oxygen Species ◽  
Vegf Mrna ◽  
Adenocarcinoma Cells ◽  
Endothelial Growth Factor ◽  
Vegf Release ◽  
Mcf 7

The inhibitory action and the possible mechanism of anticancer compound Sanguinarine (SAN) on vascular endothelial growth factor (VEGF) in human mammary adenocarcinoma cells MCF-7 were evaluated in this study. We exposed MCF-7 to SAN for 24 h, then cell viability was assessed by using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) reduction assay. Human VEGF was measured using a paired antibody quantitative ELISA kit, relative expression of VEGF mRNA was calculated using the real-time PCR studies, and the effect of SAN on the reactive oxygen species (ROS) level was detected by the flow cytometer. Treatment with SAN remarkably inhibited growth of MCF-7 cells and induced cell apoptosis. We found that VEGF release was stimulated by subtoxic concentrations of SAN and inhibited by high dose of SAN, SAN-evoked VEGF release was mimicked by low concentration of H2O2, and SAN-regulated VEGF inhibition was accompanied by increasing of ROS; these changes were abolished by antioxidant. High concentration of SAN inhibited VEGF mRNA expression in MCF-7 cultures, suggesting an effect at transcriptional level, and was also abolished by antioxidant. The present findings indicated that the regulation of VEGF expression and release from MCF-7 cells were possibly through reactive oxygen species evoked by SAN.

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