Cell cycle regulators, APC/β-catenin, NF-κB and Epstein-Barr virus in gastric carcinomas

Kim, Bomi; Byun, Sun Ju; Kim, Young A; Kim, Ji Eun; Lee, Byung Lan; Kim, Woo Ho; Chang, Mee Soo

doi:10.3109/00313020903356392

Cited by 31 publications

(21 citation statements)

References 36 publications

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“…We demonstrated increased nuclear expression of NF-B RelA along with p21 WAF1 reduction in BARF1-expressing gastric carcinoma cells. This concurs with our previous paper, which showed that EBV infection correlated with p21 WAF1 loss in immunohistochemical studies of gastric carcinomas (43). The present study showed NF-B-dependent regulation of p21 WAF1 regardless of the presence or absence of BARF1.…”

Section: Discussionsupporting

confidence: 82%

“…We suggest that BARF1 does not affect MUC1 or beta-catenin, because BARF1 transfection did not alter beta-catenin levels (data not shown). Furthermore, in our previous reports, MUC1 immunostaining was more frequently positive in EBV-negative gastric carcinoma tissues than in EBV-positive gastric carcinoma tissues (12), and the frequencies of beta-catenin alteration were similar in EBV-positive and EBV-negative gastric carcinoma tissues (12,43).…”

Section: Discussionmentioning

confidence: 99%

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Epstein-Barr Virus-Encoded BARF1 Promotes Proliferation of Gastric Carcinoma Cells through Regulation of NF-κB

Chang

Kim

Roh

et al. 2013

J Virol

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Epstein-Barr Virus-Encoded BARF1 Promotes Proliferation of Gastric Carcinoma Cells through Regulation of NF-κB

Chang

Kim

Roh

et al. 2013

J Virol

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“…Finally, it is important to mention the correlation between Epstein-Barr virus (EBV) and gastric cancer. In this regard, Kim et al [233] found that p21 and APC loss was positively correlated with EPV positive gastric carcinomas. EBV is accepted as a causative microorganism for gastric carcinoma, accounting for nearly 10% of gastric cancer cases worldwide [234] .…”

Section: Role Of Infections In Enhancing Wnt/b-catenin Pathway Signalmentioning

confidence: 99%

Role of the Wnt/β-catenin pathway in gastric cancer: An in-depth literature review

Chiurillo

2015

WJEM

270

219

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Gastric cancer remains one of the most common cancers worldwide and one of the leading cause for cancerrelated deaths. Gastric adenocarcinoma is a multifactorial disease that is genetically, cytologically and architecturally more heterogeneous than other gastrointestinal carcinomas. The identification of specific membrane, intracellular, and extracellular components of the Wnt pathway has revealed potential targets for gastric cancer therapy. High-throughput "omics" approaches will help in the search for Wnt pathway antagonist in the near future.

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“…A scoring system was established such that tumor cells in which Cx32 staining was detected in 10% or fewer cells were defined as negative and those in which staining was detected in more than 10% of cells were defined as positive [23,24]. Positively stained tissues were categorized based on localization of Cx32 expression: cell membrane and/or cytoplasm.…”

Section: Immunohistochemistry Scoring and Analysismentioning

confidence: 99%

Altered Expression and Localization of Connexin32 in Human and Murine Gastric Carcinogenesis

et al. 2010

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Background Intercellular communication via gap junctions, composed of protein subunits called connexins (Cxs), plays a key role in controlling cell growth, differentiation and carcinogenesis. Impaired gap junctional intercellular communication has been reported in various cancers and diseases. Aims We investigated Cx32 expression patterns and semiquantitatively assessed Cx32 expression in cancers and preneoplastic lesions. To determine if cell proliferation is correlated with Cx32 expression, we evaluated Ki67 expression in a gastric cancer mouse model. Methods In human and mouse, normal stomach and gastric adenocarcinoma tissues were used for immunohistochemical analyses.Results Cx32 was detected at cell-cell (intercellular) contact points in normal cells and exhibited punctate intercellular and intracytoplasmic staining in cancer cells. The frequency of Cx32 loss of expression was significantly higher in human adenocarcinomas than in normal stomach. As tumor cells were less differentiated, Cx32 expression levels and intercellular and intracytoplasmic staining were also significantly lower. The Cx32 expression pattern in the mouse gastric cancer model was similar in several important respects to that of human. In mucous metaplasia of the mouse stomach, Cx32 was mainly expressed in the cytoplasm of epithelial cells. There was also an inverse correlation between Cx32 expression and cell proliferation in mouse tumors. However, there was no difference in the levels of Cx32 mRNA between normal and cancerous tissues. Conclusions These findings suggest that altered Cx32 expression, a loss of intercellular Cx32 and a gain of intracytoplasmic Cx32 in the form of punctate ''dot'', plays an important role in the formation of gastric adenocarcinomas.

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Cell cycle regulators, APC/β-catenin, NF-κB and Epstein-Barr virus in gastric carcinomas

Cited by 31 publications

References 36 publications

Epstein-Barr Virus-Encoded BARF1 Promotes Proliferation of Gastric Carcinoma Cells through Regulation of NF-κB

Epstein-Barr Virus-Encoded BARF1 Promotes Proliferation of Gastric Carcinoma Cells through Regulation of NF-κB

Role of the Wnt/β-catenin pathway in gastric cancer: An in-depth literature review

Altered Expression and Localization of Connexin32 in Human and Murine Gastric Carcinogenesis

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