development of gastric cancer
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2022 ◽  
Vol 2022 ◽  
pp. 1-9
Author(s):  
Jiabei Xie ◽  
Lin Fu ◽  
Jianmin Zhang

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.


Bioengineered ◽  
2022 ◽  
Vol 13 (1) ◽  
pp. 1359-1376
Author(s):  
Zhonghua Cheng ◽  
Jing Hong ◽  
Nan Tang ◽  
Fenghua Liu ◽  
Shuo Gu ◽  
...  

2021 ◽  
Vol 7 (12) ◽  
pp. 114228-114244
Author(s):  
Ariane Roberta Bispo da Costa ◽  
Maria Eleonora Feracin da Silva Picoli ◽  
Raquel Machado Cavalca Coutinho ◽  
Fernando Ananias ◽  
Jacqueline Fátima Martins de Almeida Moraes

2021 ◽  
Author(s):  
Yasmin Nabiel ◽  
Ragy Shenouda ◽  
Ahmad M Sultan ◽  
Ahmed Shehata ◽  
amira M sultan

Abstract Purpose: To identify different genotypes of TLR9 -1486T/C (rs187084) in patients with gastric cancer and reveal their relation to H. pylori virulence genes (cagA, sodB, hsp60 and vacA). Methods: Patients with gastric cancer were recruited to our study, diagnosed both endoscopically and histo-pathologically. H. pylori strains were isolated from gastric samples by culture and PCR amplification of glmM gene. Virulence genes of H. pylori; cagA, sodB, Hsp60 and vacA, were detected by multiplex PCR. Blood samples were used for genotyping of TLR9 -1486T/C (rs187084) by PCR-RFLP. Results: Out of 132 patients with gastric cancer, 106 (80.3%) were positive for H. pylori by both culture and PCR. Similar number of healthy participants were recruited as controls. The prevalence of virulence genes among the isolated H. pylori were 90.6%, 70.8%, 83.0% and 95.3% for cagA, sodB, hsp60 and vacA respectively. The vacA gene alleles had a prevalence of 95.3% for vacAs1/s2, 52.8% for vacAm1 and 42.5% for vacAm2. The CC genotype of TLR9 -1486T/C had a significantly higher frequency in gastric cancer patients when compared to healthy participants (P = 0.045). Furthermore, the CC genotype demonstrated a significantly higher association with H. pylori strains carrying sodB, hsp60 and vacAm1 virulence genes (P = 0.021, P = 0.049 and P = 0.048 respectively). Conclusions: Patients with CC genotype of TLR9 -1486T/C (rs187084) are at higher risk for development of gastric cancer and its co-existence with H. pylori strains carrying sodB, hsp60 or vacAm1 virulence genes might have a synergistic effect in development of gastric cancer.


2021 ◽  
Author(s):  
Karolina Kaźmierczak-Siedlecka ◽  
Agnieszka Daca ◽  
Giandomenico Roviello ◽  
Martina Catalano ◽  
Karol Połom

AbstractCurrently, gastric cancer is one of the leading death-related cancer globally. The etiopathogenesis of gastric cancer is multifactorial and includes among others dysbiotic alterations of gastric microbiota. Molecular techniques revealed that stomach is not a sterile organ and it is resides with ecosystem of microbes. Due to the fact that the role of Helicobacter pylori infection in development of gastric cancer is established and well-studied, this paper is mainly focused on the role of other bacterial as well as viral and fungal gut microbiota imbalance in gastric carcinogenesis. Notably, not only the composition of gastric microbiota may play an important role in development of gastric cancer, but also its activity. Microbial metabolites, such as short-chain fatty acids, polyamines, N-nitroso compounds, and lactate, may significantly affect gastric carcinogenesis. Therefore, this paper discussed aforementioned aspects with the interdisciplinary insights (regarding also immunological point of view) into the association between gut microbiome and gastric carcinogenesis based on up-to-date studies.


2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Qing Li ◽  
Dachuan Zhang ◽  
Hui Wang ◽  
Jun Xie ◽  
Lei Peng ◽  
...  

Solute carrier organic anion transporter family member 4A1 (SLCO4A1-AS1), a newly discovered lncRNA, may exert effects in tumors. Since its role in gastric cancer remains obscure, we sought to explore the mechanism of SLCO4A1-AS1 in gastric cancer. The relationship among SLCO4A1-AS1, miR-149-5p, and STAT3 was detected by bioinformatics, dual luciferase analysis, and Pearson’s test, and the expressions of these genes were determined by quantitative real-time PCR and Western blot. Moreover, CCK-8, flow cytometry, wound healing assay, and Transwell analysis were performed to verify the function of SLCO4A1-AS1 in gastric cancer. Rescue experiments were used to detect the role of miR-149-5p. The expressions of SLCO4A1-AS1 and STAT3 were increased, while the expression of miR-149-5p was suppressed in gastric cancer tissues and cell lines. In addition, STAT3 expression was negatively correlated with miR-149-5p expression but was positively correlated with SLCO4A1-AS1 expression. Overexpression of SLCO4A1-AS1 promoted cell viability, migration, invasion, and STAT3 expression but suppressed apoptosis, while knockdown of SLCO4A1-AS1 had the opposite effect. SLCO4A1-AS1 bound to miR-149-5p and targeted STAT3. Moreover, miR-149-5p mimic inhibited the malignant development of gastric cancer cells and obviously reversed the function of SLCO4A1-AS1 overexpression. Our research reveals that abnormally increased SLCO4A1-AS1 expression may be an important molecular mechanism in the development of gastric cancer.


2021 ◽  
Vol 49 (9) ◽  
pp. 030006052110331
Author(s):  
Shasha Liu ◽  
Yang Zhao ◽  
Huan Liu ◽  
Xing Zhao ◽  
Xingbin Shen

Objective Identifying novel biomarkers involved in the development of gastric cancer (GC) can provide potential therapeutic strategies and improve clinical prognosis. miR-301-3p and Cx43 are reportedly dysregulated in GC. miR-301-3p and Cx43 interaction, and their functions in GC progression, are still poorly understood. Methods The expression levels of miR-301-3p and Cx43 in GC tissues and cell lines with various differentiation degrees were evaluated by RT-qPCR. The interaction between miR-301-3p and Cx43 was assessed by dual-luciferase reporter assays. CCK8 and Transwell assays were employed to assess the effects of the miR-301-3p- Cx43 axis on GC cell proliferation, migration, and invasion. Results Cx43 was significantly downregulated in GC tissues and cell lines, while miR-301-3p expression was negatively correlated with Cx43 mRNA levels. The expression levels of Cx43 and miR-301-3p were closely associated with the differentiation, TNM stage, vascular invasion, and lymph node metastasis status of GC patients. Cx43 overexpression could suppress the proliferation, migration, and invasion of GC cells. Cx43 mRNA is a direct target of miR-301-3p, and transfection of an miR-301-3p mimic could reverse the inhibitory effects of Cx43. Conclusion The miR-301-3p- Cx43 axis is involved in the development and progression of GC by affecting the proliferation, migration, and invasion of GC cells.


2021 ◽  
Author(s):  
Norma Sánchez-Zauco ◽  
Erandi Pérez-Figueroa ◽  
Carmen Maldonado-Bernal

Gastric cancer is one of the types of cancer that is associated with Helicobacter pylori infection. The infection starts in childhood, and 50–90% of the population in the world is infected. The clinical symptoms can be stomach pain, gastritis, atrophy gastric, and only 2–3% of the infected population developed gastric cancer. The majority of gastric cancers are adenocarcinomas. From Lauren’s histological classification, gastric cancer is divided into two large groups: intestinal and diffuse. The cells that gives rise to them are different and the epidemiologic features and diagnosis are different according to gender and age; however; the survival rate is approximately of 5-years. Surgery is the only radical treatment, but the adjuvant treatment is chemotherapy and radiotherapy which unfortunately lead to only a modest survival benefit. On this review, we describe the major risk factors associated with the bacteria: cagPAI, CagA, VacA, HOPs, as well as host immune and inflammatory responses: immune cells, Toll-like receptors, cytokines, immune signal pathway, genetic predisposition, such as single nucleotide polymorphisms (SNP’s) and environmental factors: age, high salt intake, diets low in fruit and vegetables, alcohol intake, and tobacco use. Finally, we included the interaction of all factors for the development of gastric cancer. Knowing and understanding the role of all factors in the development of gastric cancer will allow the implementation of better therapies and improve patient prognosis.


Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1293
Author(s):  
Ting-Yu Lin ◽  
Wen-Hsi Lan ◽  
Ya-Fang Chiu ◽  
Chun-Lung Feng ◽  
Cheng-Hsun Chiu ◽  
...  

Conventionally, statins are used to treat high cholesterol levels. They exhibit pleiotropic effects, such as the prevention of cardiovascular disease and decreased cancer mortality. Gastric cancer (GC) is one of the most common cancers, ranking as the third leading global cause of cancer-related deaths, and is mainly attributed to chronic Helicobacter pylori infection. During their co-evolution with hosts, H. pylori has developed the ability to use the cellular components of the host to evade the immune system and multiply in intracellular niches. Certain H. pylori virulence factors, including cytotoxin-associated gene A (CagA), vacuolating cytotoxin A (VacA), and cholesterol-α-glucosyltransferase (CGT), have been shown to exploit host cholesterol during pathogenesis. Therefore, using statins to antagonize cholesterol synthesis might prove to be an ideal strategy for reducing the occurrence of H. pylori-related GC. This review discusses the current understanding of the interplay of H. pylori virulence factors with cholesterol and reactive oxygen species (ROS) production, which may prove to be novel therapeutic targets for the development of effective treatment strategies against H. pylori-associated GC. We also summarize the findings of several clinical studies on the association between statin therapy and the development of GC, especially in terms of cancer risk and mortality.


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