p53, a potential predictor of<i>Helicobacter pylori</i>infection-associated gastric carcinogenesis?

Li, Nianshuang; Xie, Chuan; Lü, Nonghua

doi:10.18632/oncotarget.11414

Cited by 38 publications

(23 citation statements)

References 103 publications

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“…and signaling pathways (PI3 kinase‐AKT, β‐catenin‐WNT, and NF‐κB pathways, etc.) were confirmed to play an important role in H. pylori pathogenesis . However, a database‐based comprehensive analysis of genes and signaling pathways involved in H. pylori pathogenesis is lacking.…”

Section: Introductionmentioning

confidence: 99%

Analysis of key genes and signaling pathways involved in Helicobacter pylori‐associated gastric cancer based on The Cancer Genome Atlas database and RNA sequencing data

Liu

et al. 2018

Helicobacter

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Section: Introductionmentioning

confidence: 99%

Analysis of key genes and signaling pathways involved in Helicobacter pylori‐associated gastric cancer based on The Cancer Genome Atlas database and RNA sequencing data

Liu

et al. 2018

Helicobacter

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“…Deregulation of p53-mediated cellular processes, such as apoptosis and cell cycle control signaling pathways, have been associated with the progression of gastric cancer [ 12 , 26 , 29 , 30 ]. In the current study, the TCGA database was interrogated to identify deregulated p53-associated cell cycle and apoptosis genes in gastric cancer.…”

Section: Discussionmentioning

confidence: 99%

Inverse expression of survivin and reprimo correlates with poor patient prognosis in gastric cancer

Cerda-Opazo

Valenzuela-Valderrama

Wichmann

et al. 2018

Oncotarget

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BACKGROUNDThe objective of the study was to determine the relationship between Survivin and Reprimo transcript/protein expression levels, and gastric cancer outcome.METHODSIn silico correlations between an agnostic set of twelve p53-dependent apoptosis and cell-cycle genes were explored in the gastric adenocarcinoma TCGA database, using cBioPortal. Findings were validated by regression analysis of RNAseq data. Separate regression analyses were performed to assess the impact of p53 status on Survivin and Reprimo. Quantitative reverse-transcription PCR (RT-qPCR) and immunohistochemistry confirmed in silico findings on fresh-frozen and paraffin-embedded gastric cancer tissues, respectively. Wild-type (AGS, SNU-1) and mutated p53 (NCI-N87) cell lines transfected with pEGFP-Survivin or pCMV6-Reprimo were evaluated by RT-qPCR and Western blotting. Kaplan-Meier method and Long-Rank test were used to assess differences in patient outcome.RESULTScBioPortal analysis revealed an inverse correlation between Survivin and Reprimo expression (Pearson’s r= −0.3, Spearman’s ρ= −0.55). RNAseq analyses confirmed these findings (Spearman’s ρ= −0.37, p<4.2e-09) and revealed p53 dependence in linear regression models (p<0.05). mRNA and protein levels validated these observations in clinical samples (p<0.001). In vitro analysis in cell lines demonstrated that increasing Survivin reduced Reprimo, while increasing Reprimo reduced Survivin expression, but only did so in p53 wild-type gastric cells (p<0.05). Survivin-positive but Reprimo-negative patients displayed shorter overall survival rates (p=0.047, Long Rank Test) (HR=0.32; 95%IC: 0.11-0.97; p=0.044).CONCLUSIONSTCGA RNAseq data analysis, evaluation of clinical samples and studies in cell lines identified an inverse relationship between Survivin and Reprimo. Elevated Survivin and reduced Reprimo protein expression correlated with poor patient prognosis in gastric cancer.

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“…Inactivation and accumulation of p53 is a hallmark of carcinogenesis, including GC, in which higher p53 levels in malignant tissue are associated with poor prognosis (Yildirim et al, 2015;Zhou et al, 2016). H. pylori induction of p53 expression has been described in chronic gastritis and preneoplasic lesions (such as intestinal, metaplasia and dysplasia in adults), especially those associated with CagA-positive strains (Teh et al, 2002;Li et al, 2016). Pediatric studies assessed in this review showed contradictory results, with p53 overexpressed in gastric tissue of H. pylori infected children, and directly correlated with gastritis, the magnitude of inflammatory cell infiltration and H. pylori tissue density in two studies (Ozturk et al, 2005;Saf et al, 2015); while on the other hand two other studies showed similar expression levels in infected and non-infected children (Nardone et al, 2001;Villarreal-Calderon et al, 2014).…”

Section: Transcription Factorsmentioning

confidence: 99%

Gastric Damage and Cancer-Associated Biomarkers in Helicobacter pylori-Infected Children

et al. 2020

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Helicobacter pylori (H. pylori) is well-known to be involved in gastric carcinogenesis, associated with deregulation of cell proliferation and epigenetic changes in cancerrelated genes. H. pylori infection is largely acquired during childhood, persisting long-term in about half of infected individuals, a subset of whom will go on to develop peptic ulcer disease and eventually gastric cancer, however, the sequence of events leading to disease is not completely understood. Knowledge on carcinogenesis and gastric damage-related biomarkers is abundant in adult populations, but scarce in children. We performed an extensive literature review focusing on gastric cancer related biomarkers identified in adult populations, which have been detected in children infected with H. pylori. Biomarkers were related to expression levels (RNA or protein) and/or methylation levels (DNA) in gastric tissue or blood of infected children as compared to non-infected controls. In this review, we identified 37 biomarkers of which 24 are over expressed, three are under expressed, and ten genes are significantly hypermethylated in H. pylori-infected children compared to healthy controls in at least 1 study. Only four of these biomarkers (pepsinogen I, pepsinogen II, gastrin, and SLC5A8) have been studied in asymptomatically infected children. Importantly, 13 of these biomarkers (β-catenin, C-MYC, GATA-4, DAPK1, CXCL13, DC-SIGN, TIMP3, EGFR, GRIN2B, PIM2, SLC5A8, CDH1, and VCAM-1.) are consistently deregulated in infected children and in adults with gastric cancer. Future studies should be designed to determine the clinical significance of these changes in infection-associated biomarkers in children and their persistence over time. The effect of eradication therapy over these biomarkers in children if proven significant, could lead to modifications in treatment guidelines for younger populations, and eventually promote the development of preventive strategies, such as vaccination, in the near future.

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p53, a potential predictor ofHelicobacter pyloriinfection-associated gastric carcinogenesis?

Cited by 38 publications

References 103 publications

Analysis of key genes and signaling pathways involved in Helicobacter pylori‐associated gastric cancer based on The Cancer Genome Atlas database and RNA sequencing data

Analysis of key genes and signaling pathways involved in Helicobacter pylori‐associated gastric cancer based on The Cancer Genome Atlas database and RNA sequencing data

Inverse expression of survivin and reprimo correlates with poor patient prognosis in gastric cancer

Gastric Damage and Cancer-Associated Biomarkers in Helicobacter pylori-Infected Children

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