4.3 Article

Peroxiredoxin V Silencing Elevates Susceptibility to Doxorubicin-induced Cell Apoptosis via ROS-dependent Mitochondrial Dysfunction in AGS Gastric Cancer Cells

Journal

ANTICANCER RESEARCH
Volume 41, Issue 4, Pages 1831-1840

Publisher

INT INST ANTICANCER RESEARCH
DOI: 10.21873/anticanres.14949

Keywords

Peroxiredoxin V; reactive oxygen species; apoptosis; mitochondria; gastric cancer

Categories

Funding

  1. 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

Primary Rating

4.3
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available