Stomach cancer is the second largest cause of
cancer-related mortality globally, and it continues to be a reason for worry today. Inhalation of the
stomach cancer risk factor H. pylori produces large levels of
reactive oxygen species (ROS). When combined with
glutathione reductase,
glutathione peroxidase 3 (GPX3) catalyzes the reduction of
hydrogen peroxide and
lipid peroxides. To get a better understanding of the GPX3 gene's role in the illness, the researchers used quantitative real-time RT-PCR to examine the gene's expression and regulation in
gastric cancer cell lines, original
gastric cancer samples, and 45 normal stomach mucosa adjacent to
malignancies. According to the research, GPX3 expression was decreased or silenced in eight of nine
cancer cell lines and 83 percent of
gastric cancer samples (90/108) as compared to normal gastric tissues in the vicinity of the
tumor (P < 0.0001). It was found that 60 percent of
stomach cancer samples exhibited
DNA hypermethylation after analyzing the GPX3 promoter (P=0.007) (a methylation level of more than 10 percent, as measured by
bisulfite pyrosequencing). In stomach
tumors, we found a statistically significant reduction in the amount of GPX3
DNA copies (P < 0.001). The gene expression of SNU1 and MKN28 cells was restored
after treatment with 5-Aza-2'
Deoxycytidine to reduce GPX3 promoter methylation. Genetic and epigenetic alterations lead GPX3 to be dysfunctional in
gastric cancer. This indicates that the systems that regulate ROS have been disrupted, and GPX3 may be implicated in the development of
gastric cancer, as shown by our results when evaluated alone and in combination.