Altered expression of Skp2, c-Myc and p27 proteins but not mRNA after H. pylori eradication in chronic gastritis

Kim, Sung S.; Meitner, Patricia A.; Konkin, Tamako; Cho, Young S; Resnick, Murray B.; Moss, Steven F.

doi:10.1038/modpathol.3800476

Cited by 39 publications

(33 citation statements)

References 47 publications

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“…Transfection of p27 kip1 into cell lines increased susceptibility to H. pylori induced apoptosis [37], while H. pylori infection of p27 kip1 knockout mice led to increased rates of dysplasia and gastric cancer at 75 weeks postinfection [38 ]. These findings are also being translated into the clinical arena as p27 kip1 protein expression is increased in human gastric antrum following H. pylori eradication [39]. The gastric mucosal growth factor Reg is another important factor in gastric carcinogenesis.…”

Section: Host Factorsmentioning

confidence: 94%

Helicobacter pylori and gastric cancer

Pritchard

2006

Current Opinion in Gastroenterology

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Section: Host Factorsmentioning

confidence: 94%

Helicobacter pylori and gastric cancer

Pritchard

2006

Current Opinion in Gastroenterology

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“…These cytokines recruit neutrophils and macrophages to sites of inflammation, but prolonged exposure to these cytokines has been linked clinically to increased gastric cancer risk (58)(59)(60)(61)(62)(63). H. pylori infection has been associated with increased IL-8 expression and decreased p27 levels (64). Both reduced p27 levels and increased IL-8 levels have been shown to mediate decreased apoptosis (65)(66)(67)(68).…”

Section: Origin Alters Transcription and Virulence Of H Pylorimentioning

confidence: 99%

Phylogeographic Origin of Helicobacter pylori Determines Host-Adaptive Responses upon Coculture with Gastric Epithelial Cells

et al. 2013

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g While Helicobacter pylori infects over 50% of the world's population, the mechanisms involved in the development of gastric disease are not fully understood. Bacterial, host, and environmental factors play a role in disease outcome. To investigate the role of bacterial factors in H. pylori pathogenesis, global gene expression of six H. pylori isolates was analyzed during coculture with gastric epithelial cells. Clustering analysis of six Colombian clinical isolates from a region with low gastric cancer risk and a region with high gastric cancer risk segregated strains based on their phylogeographic origin. One hundred forty-six genes had increased expression in European strains, while 350 genes had increased expression in African strains. Differential expression was observed in genes associated with motility, pathogenicity, and other adaptations to the host environment. European strains had greater expression of the virulence factors cagA, vacA, and babB and were associated with increased gastric histologic lesions in patients. In AGS cells, European strains promoted significantly higher interleukin-8 (IL-8) expression than did African strains. African strains significantly induced apoptosis, whereas only one European strain significantly induced apoptosis. Our data suggest that gene expression profiles of clinical isolates can discriminate strains by phylogeographic origin and that these profiles are associated with changes in expression of the proinflammatory and protumorigenic cytokine IL-8 and levels of apoptosis in host epithelial cells. These findings support the hypothesis that bacterial factors determined by the phylogeographic origin of H. pylori strains may promote increased gastric disease.

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“…Kim et al [65] investigated the expression of MYC protein and mRNA in 22 patients with chronic gastritis who had been successfully treated for H pylori. Two endoscopic antral biopsies were taken before and 2 mo after H pylori eradication.…”

Section: Myc and Gastric Carcinogenesismentioning

confidence: 99%

“…These authors found that MYC expression was significantly higher in those lesions of type Ⅲ intestinal metaplasia and dysplasia Ⅱ-Ⅲ with cagA than in those without cagA. Nardone et al [64] also suggested that the increased prevalence of MYC expression was in agreement with the high prevalence of cagA positivity seen in the population studied.Kim et al [65] investigated the expression of MYC protein and mRNA in 22 patients with chronic gastritis who had been successfully treated for H pylori. Two endoscopic antral biopsies were taken before and 2 mo after H pylori eradication.…”

mentioning

confidence: 99%

MYC and gastric adenocarcinoma carcinogenesis

Calcagno¹,

Leal²,

Assumpção³

et al. 2008

WJG

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MYC is an oncogene involved in cell cycle regulation, cell growth arrest, cell adhesion, metabolism, ribosome biogenesis, protein synthesis, and mitochondrial function. It has been described as a key element of several carcinogenesis processes in humans. Many studies have shown an association between MYC deregulation and gastric cancer. MYC deregulation is also seen in gastric preneoplastic lesions and thus it may have a role in early gastric carcinogenesis. Several studies have suggested that amplification is the main mechanism of MYC deregulation in gastric cancer.In the present review, we focus on the deregulation of the MYC oncogene in gastric adenocarcinoma c a r c i n o g e n e s i s , i n c l u d i n g i t s a s s o c i a t i o n w i t h Helicobacter pylori (H pylori ) MYC AND CANCERMYC gene was found to be the cellular homolog of retroviral v-myc oncogene about 30 years ago [12][13][14] . It is located on chromosomal region 8q24.1, has 3 exons [15,16] and encodes a nuclear phosphoprotein [17] . MYC has to heteromerize with MAX, a protein expressed constitutively, to acquire DNA-binding activity. MYC/MAX dimmers are made viable by a basic region helix-loop-helix leucine-zipper motif (bHLHZip), conserved sequences in the carboxyl terminus of both proteins. MYC/MAX dimmers bind to E-box sequence CACGTG in the promoters of specific target genes and stimulate their transcription [18] . MYC has an effect on up to about 15% of genes in genomes of many organisms, from flies to humans [19] . Groups of genes involved in cell cycle regulation, metabolism, ribosome biogenesis, protein synthesis, and mitochondrial function are over-represented in the Myc target gene network.MYC also consistently represses genes involved in cell growth arrest and cell adhesion [20] . Dominguez-Sola et al [21] recently showed that Myc interacts with the prereplicative complex and localizes to early sites of DNA synthesis. Thus, it also has a direct role in the control of DNA replication.MYC regulates transcription from its targets through several mechanisms, including recruitment of histone acetylases, chromatin modulating proteins, basal transcription factors and DNA methyltransferase [22][23][24][25][26] . Protein products of MYC target genes g o on to mediate the downstream effects of MYC on cell biology. MYC is then rapidly degraded, and the pathway switches to a transcriptionally repressive state when MAX dimerizes with a group of related bHLH-Zip proteins, the MAD family, that act as MYC antagonists [27] ( Figure 1).MYC expression might be regulated transcriptionally (initiation and elongation), post-transcriptionally (mRNA stability and translation) or post-translationally (protein stability) [28] . MYC is generally recognized as an important regulator of proliferation, growth, differentiation and apoptosis [29,30] . Therefore, it is also accepted that the deregulation of MYC expression is a major event in cancer pathogenesis or progression. Deregulated expression of a wild-type MYC protein is suff...

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Altered expression of Skp2, c-Myc and p27 proteins but not mRNA after H. pylori eradication in chronic gastritis

Cited by 39 publications

References 47 publications

Helicobacter pylori and gastric cancer

Helicobacter pylori and gastric cancer

Phylogeographic Origin of Helicobacter pylori Determines Host-Adaptive Responses upon Coculture with Gastric Epithelial Cells

MYC and gastric adenocarcinoma carcinogenesis

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