Journal
ANTICANCER RESEARCH
Volume 41, Issue 4, Pages 1831-1840Publisher
INT INST ANTICANCER RESEARCH
DOI: 10.21873/anticanres.14949
Keywords
Peroxiredoxin V; reactive oxygen species; apoptosis; mitochondria; gastric cancer
Categories
Funding
- national natural science foundation of China [31760330]
Ask authors/readers for more resources
The study suggests that Prx V knockdown may significantly increase DOX-induced apoptosis by aggravating intracellular ROS accumulation, and also activates mitochondria-dependent apoptotic signaling pathways.
Background/Aim: Peroxiredoxin V (Prx V) plays crucial roles in cellular apoptosis and proliferation in various cancer cells by regulating the cellular reactive oxygen species (ROS) levels. Materials and Methods: Here, we examined the possible regulatory effects of Prx V on doxorubicin (DOX)-induced cellular apoptosis and its mechanisms in the human gastric adenocarcinoma cell line (AGS cells). Results: Our findings suggest that Prx V knockdown may significantly increase the DOX-induced apoptosis by aggravating intracellular ROS accumulation. We also found that DOX-induced mitochondrial ROS levels and membrane permeability were significantly higher in short hairpin Prx V cells than in mock cells, and these phenomena were dramatically reversed by ROS scavenger treatment. Prx V knockdown also significantly upregulated the cleaved caspase 9, 3, and B-cell lymphoma 2 (Bcl2)associated agonist of cell death/Bcl2 protein expression levels, suggesting that Prx V knockdown activates mitochondria-dependent apoptotic signaling pathways. Conclusion: Taken together, this study suggests that Prx V may be a strong molecular target for gastric cancer (GC) chemotherapy, and further elucidates the role of Prx V in oxidative stress-induced cell apoptosis.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available