H. pylori modifies methylation of global genomic DNA and the gastrin gene promoter in gastric mucosal cells and gastric cancer cells

2017 ◽  
Vol 108 ◽  
pp. 129-136 ◽  
Author(s):  
Yuan Xie ◽  
Jian Jiang Zhou ◽  
Yan Zhao ◽  
Ting Zhang ◽  
Liu Zheng Mei
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Genomic Dna ◽  
Gene Promoter ◽  
Gastric Cancer Cells ◽  
Gastric Mucosal Cells ◽  
Mucosal Cells ◽  
H Pylori

scholarly journals Gramicidin inhibits human gastric cancer cell proliferation, cell cycle and induced apoptosis

2019 ◽  
Vol 52 (1) ◽  
Author(s):  
Tingting Chen ◽  
Yong Wang ◽  
Yang Yang ◽  
Kaikai Yu ◽  
Xiangliao Cao ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
High Morbidity ◽  
Peptide Antibiotic ◽  
Human Gastric Cancer ◽  
M Cell ◽  
Gastric Cancer Cells ◽  
Gastric Mucosal Cells ◽  
Mucosal Cells

Abstract Background Gastric cancer is a common malignant tumor with high morbidity and mortality worldwide, which seriously affects human health. Gramicidin is a short peptide antibiotic which could be used for treating infection induced by bacteria or fungi. However, the anti-cancer effect of gramicidin on gastric cancer cells and its underlying mechanism remains largely unknown. Results Gastric cancer cells SGC-7901, BGC-823 and normal gastric mucosal cells GES-1 were treated with different concentrations of gramicidin respectively. The results of CCK-8 experiment revealed cellular toxicity of gramicidin to cancer cells while cell colony formation assay showed that gramicidin significantly inhibited the proliferation of gastric cancer cells, but had little effect on normal gastric mucosal cells. In addition, the wound healing assay showed that gramicidin inhibited the migration of SGC-7901 cell. Meanwhile, apoptosis and cell cycle analysis revealed that gramicidin induced cell apoptosis with G2/M cell cycle inhibition. Furthermore, western blot analysis demonstrated that gramicidin down-regulated the expression of cyclinD1 and Bcl-2 as well as the FoxO1 phosphorylation. Conclusions The current study illustrated the anti-tumor activity of gramicidin on gastric cancer cells, providing a possibility for gramicidin to be applied in clinical practice for the treatment of gastric cancer.

scholarly journals The Association of EBV and Gastric Cancer

2021 ◽  
Author(s):  
Xuming Wang ◽  
Tian Liu ◽  
Lijuan Yu ◽  
Wenfa Mo ◽  
Longkuan Xu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Caspase 3 ◽  
Gastric Cancer Cells ◽  
Gastric Mucosal Cells ◽  
Expression Levels ◽  
Mucosal Cells ◽  
Gastric Cancer Patients ◽  
Cancer Tissues

Abstract The present study aimed to investigate the clinicopathological features of EBV positive and EBV negative gastric cancer patients and the expression levels of proliferative, apoptotic and cell signaling proteins in tissues samples from these patients. The biological role of EBV infection was assessed in gastric cancer. Results: EBV was localized in the nuclei of gastric cancer cells (positive rate 6.86%). The infection rate of EBV in normal gastric mucosal cells, which were adjacent to cancer tissues, was 0. The difference noted was significant (P = 0. 023). The expression levels of caspase-3 (P = 0.0423), FASL (P = 0.00297) and cyclin D1 (P = 0.0345) proteins were significantly different in EBV positive and negative gastric cancer tissues. When the parameters gender, age, Lauren classification, histological grade, early and advanced tumor stage, vascular and nerve invasion, TNM grade and survival status were compared, the maximum tumor diameter, number of lymph node metastasis, caspase-8, Ki67 and P53 protein expression did not reveal significant differences. Bcl-2 protein expression was positive in only one gastric cancer cell sample and negative in the other gastric cancer cell samples as well as in the corresponding normal gastric mucosal epithelial cells. However, significant differences were noted with regard to the positive expression of Bcl-2 in the immune cells of gastric cancer and adjacent tissues (P = 1.17749E-39). The expression levels of Bcl-2 in the immune cells of EBV positive and EBV negative gastric cancer tissues were not significantly different. The expression levels of caspase-8, caspase-3, FASL, Ki67, cyclin D1 and P53 proteins in gastric cancer cells were significantly different compared to those of normal gastric mucosal cells derived from adjacent tissues (P < 0.05). These findings were noted in both EBV positive and/or EBV negative gastric cancer cases (P < 0.05). The survival time of the patients with EBV positive gastric cancer was higher than that of the patients with EBV negative gastric cancer, whereas the differences were not significantly different. The aforementioned results suggested that the EBV virus may directly infect cancerous cells but not normal gastric mucosal cells. With the exception of caspase-3, the expression levels of the proteins FASL and cyclin D1 were closely associated with EBV-positive gastric cancer. EBV did not have a specific effect on the expression of the signaling molecules associated with proliferation and apoptosis of gastric cancer cells. Its effect on gastric cancer cells may be associated with other factors and requires further discussion. No significant differences were noted in the clinicopathological features of EBV positive compared to those of EBV negative gastric cancer patients. However, the prognosis of EBV positive gastric cancer patients was better than that of EBV negative gastric cancer patients. The mechanism of action associated with these processes requires further verification.

The regulatory role of exosomal CagA and microRNAs derived from H. pylori-related gastric cancer cells on signaling pathways related to cancer development: a bioinformatics aspect

2020 ◽  
Vol 29 (6) ◽  
pp. 1295-1312
Author(s):  
Nazila Bostanshirin ◽  
Ahmad Bereimipour ◽  
Mohammad ali Pahlevan Neshan ◽  
Mina Aghasafi ◽  
Romina Mehtararaghinia ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Cancer Development ◽  
Regulatory Role ◽  
Gastric Cancer Cells ◽  
H Pylori

scholarly journals H. pylori-Induced Apoptosis in Human Gastric Cancer Cells Mediated via the Release of Apoptosis-Inducing Factor from Mitochondria

Helicobacter ◽  
2008 ◽  
Vol 13 (6) ◽  
pp. 506-517 ◽  
Author(s):  
Hassan Ashktorab ◽  
Rod H. Dashwood ◽  
Mohaiza M. Dashwood ◽  
Syed I. Zaidi ◽  
Stephen M. Hewitt ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
H Pylori ◽  
Induced Apoptosis ◽  
Apoptosis Inducing Factor

Lotus tetragonolobus and Maackia amurensis lectins influence phospho-IκBα, IL-8, Lewis b and H type 1 glycoforms levels in H. pylori infected CRL-1739 gastric cancer cells

2018 ◽  
Vol 63 (1) ◽  
pp. 205-211 ◽  
Author(s):  
Iwona Radziejewska ◽  
Małgorzata Borzym-Kluczyk ◽  
Katarzyna Leszczyńska ◽  
Joanna Wosek ◽  
Anna Bielawska
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Gastric Cancer Cells ◽  
Maackia Amurensis ◽  
H Pylori

scholarly journals Autophagy induced by H. pylori VacA regulated the survival mechanism of the SGC7901 human gastric cancer cell line

2021 ◽  
Author(s):  
Juan Luo ◽  
Luyan Bai ◽  
Jun Tao ◽  
Yu Wen ◽  
Mingke Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cell Line ◽  
Molecular Mechanism ◽  
Gastric Cancer Cell ◽  
Gastric Cancer Cell Line ◽  
Cancer Cell Line ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
H Pylori

Abstract Background Vacuolating cytotoxin (VacA) is an important virulence factor of Helicobacter pylori (H. pylori). It was previously believed that VacA can trigger the cascade of apoptosis on mitochondria to lead to cell apoptosis. Recently, it was found that VacA can induce autophagy. However, the molecular mechanism by which VacA induces autophagy is largely unknown. Objective We aimed to explore the molecular mechanism of autophagy induced by H. pylori in gastric cancer cells and the effect of autophagy on the survival of gastric cancer cells. Methods The autophagy of human gastric cancer cell line SGC7901 was detected by Western blot and RT-PCR in the treatment of VacA protein of H. pylori. The relationship between autophagy and reactive oxygen species (ROS) in the proliferation of gastric cancer cells were studied by gene expression silences (siRNA) and CM-H2DCFDA (DCF) staining. Results The results showed that VacA protein secreted by H. pylori in the supernatant stimulated autophagy in SGC7901 cells. After VacA protein treatment, the mRNA expressions of BECN1, ATG7 and PIK3C3, were up-regulated. ATG7 silencing by siRNA inhibited VacA-induced autophagy. Furthermore, our data demonstrated that VacA protein increased ROS levels. Addition of the antioxidant N-acetyl-l-cysteine (NAC) suppressed the levels of ROS, leading to inhibition of autophagy. Conclusions H. pylori VacA is a key toxin that induces autophagy by increased ROS levels. And our findings demonstrated that VacA significantly inhibited proliferation in SGC7901 cells.

Long Noncoding RNA NEAT1 Promotes Tumorigenesis in H. Pylori Gastric Cancer By Sponging miR-30a To Regulate COX-2/BCL9 Pathway

2021 ◽  
Author(s):  
Xiwu Rao ◽  
Ningning Liu ◽  
Ru Jia ◽  
Yuanyuan Feng ◽  
Zhaozhou Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cell Counting ◽  
Luciferase Assay ◽  
Gastric Cancer Cells ◽  
Dual Luciferase Assay ◽  
Cox 2 ◽  
H Pylori ◽  
Cancer Tissues ◽  
Lncrna Neat1

Abstract Background: Helicobacter pylori (H. pylori) is a carcinogenic factor for gastric cancer. Our previous study demonstrated that H. pylori decreased the expression of microRNA(miRNA)-30a to promote the tumorigenesis in gastric cancer. However, the upstream regulatory mechanism of miR-30a hasn’t well-elucidated. In this study, we found the long non‑coding RNA (lncRNA) NEAT1 may sponge miR-30a to regulate COX-2/BCL9 pathway. Methods: The expression of NEAT1 was detected in gastric cancer tissues and tumour adjacent tissues by fluorescence in-situ hybridization(FISH) analysis and RT-qPCR. LncRNA-miRNA interaction networks were constructed using the RNAhybird and Starbase v.2.0. and then validated using dual-luciferase assay. The effects of NEAT1 dysregulation on the proliferative, migratory and invasive abilities of H. pylori filtrate infected gastric cancer cells were observed by cell counting kit-8 (CCK-8), colony formation, wound healing test and transwell assays. Western blot and RT-qPCR were performed to detect protein and RNA expression. The Immunohistochemistry(IHC) was carried out to analyze the location and expression of COX-2 and BCL9Results: FISH and RT-qPCR demonstrated that the expression of NEAT1 was up-regulated in gastric cancer tissues, especially in H. pylori gastric cancer tissues, and the expression of NEAT1 is negatively correlated with miR-30a(miR-30a-3p, miR-30a-5p). The proliferation, migration and invasion of H. pylori filtrate infected gastric cancer cells could be largely enhanced by the up-regulation of NEAT1, while the downregulation of NEAT1 decreased these abilities, and miR-30a could reverse the effect of NEAT1 on these abilities. Dual-luciferase assay identified that NEAT1 directly targeted miR-30a(miR-30a-3p, miR-30a-5p).Due to miR-30a(miR-30a-3p, miR-30a-5p) negatively regulated the expression of downstream COX-2 and BCL9, NEAT1 was identified to indirectly upregulate the expression of COX-2 and BCL9.IHC showed that the expression of COX-2 and BCL9 were increased in H. pylori gastric cancer tissues.Conclusion: The study demonstrated that lncRNA NEAT1 may act as a promoter oftumorigenesis in H. pylori gastric cancer, by sponging miR-30a(miR-30a-3p, miR-30a-5p) to regulate COX-2/BCL9 pathway.

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