Abstract
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.
Highlights
Gastric cancer is the most common kind of malignancy discovered throughout the globe
Quantitative real-time polymerase chain reaction (PCR) and immunohistochemistry showed by Zhou et al using pyrosequencing that hypermethylation of glutathione peroxidase 3 (GPX3) in gastric cancer among 108 American patients was linked to decreased levels of gene and protein expression. e authors in [5] found that the GPX3 promoter was hyperethylated and that the protein expression of GPX3 was decreased in tissue samples from 22 Korean gastric cancer patients when compared to seven healthy individuals utilizing bisulfite sequencing and immunohistochemistry
A new research shows that GPX3 inhibits the growth and spread of stomach cancer
Summary
Gastric cancer is the most common kind of malignancy discovered throughout the globe. Ere were varying views on whether or not abnormal GPX3 methylation and expression were present in gastric cancer, but it was generally agreed upon that they were. Quantitative real-time PCR (qRT-PCR) and immunohistochemistry showed by Zhou et al using pyrosequencing that hypermethylation of GPX3 in gastric cancer among 108 American patients was linked to decreased levels of gene and protein expression (immunofluorescence). E authors in [5] found that the GPX3 promoter was hyperethylated and that the protein expression of GPX3 was decreased in tissue samples from 22 Korean gastric cancer patients when compared to seven healthy individuals utilizing bisulfite sequencing and immunohistochemistry. When researchers examined the GPX3 expression in blood and tissue samples from 40 Chinese patients with that of 50 healthy controls, they found that there was no difference.
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