The Origins of Gastric Cancer From Gastric Stem Cells: Lessons From Mouse Models

Hayakawa, Yoku; Fox, James G.; Wang, Yichen

doi:10.1016/j.jcmgh.2017.01.013

Cited by 55 publications

(55 citation statements)

References 103 publications

(184 reference statements)

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“…Surface mucous epithelial cells in the gastric mucosa are columnar, and epithelial cells in the glands are cuboidal, but their morphological details and cellular makeup differ (16,17).…”

Section: Introductionmentioning

confidence: 99%

“…Stem cells in the corpus express Sox2, Troy, Mist1, and eR1, whereas stem cells in the pyloric antrum express Sox2, Lgr5, CCK2R, eR1, Axin2, and Mist1 (18-25). Mouse model studies have shown that oncogenic events in gastric stem cells can frequently lead to carcinogenesis, although mutations targeted to chief cells also can cause these cells to dedifferentiate and acquire the potential to grow and regenerate gastric glands, sometimes forming metaplasia (17,21,22,(26)(27)(28)(29)(30).…”

Section: Introductionmentioning

confidence: 99%

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YAP/TAZ Initiates Gastric Tumorigenesis via Upregulation of MYC

et al. 2018

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“…Surface mucous epithelial cells in the gastric mucosa are columnar, and epithelial cells in the glands are cuboidal, but their morphological details and cellular makeup differ (16,17).…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

YAP/TAZ Initiates Gastric Tumorigenesis via Upregulation of MYC

et al. 2018

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“…Gastric cancer, primarily associated with Helicobacter pylori infectious inflammation, is one of the most common fatal cancers worldwide. 1,2 Aspirin exhibits a protective effect in gastrointestinal cancer, 3 including gastric cancer development, due to its antiinflammatory and antiplatelet functions, including induction of apoptosis 4 and inhibition of angiogenesis. 5 Previous meta-analyses have reported a potential relationship between aspirin use and prevention of gastric cancer.…”

Section: Introductionmentioning

confidence: 99%

Effect of aspirin use on gastric cancer incidence and survival: A systematic review and meta‐analysis

et al. 2019

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Background and Aim A number of recent studies have been published evaluating the chemopreventive effect of aspirin against gastric cancer, and an updated meta‐analysis is required to evaluate this relationship further. This study presents a meta‐analysis of studies examining the effect of aspirin on gastric cancer incidence and death. Methods The PUBMED and Cochrane Central Registration of Controlled Trials databases were searched for eligible studies published up to December 2018. Pooled risk ratios for gastric cancer incidence and death in aspirin users versus nonusers were determined using fixed‐ and random‐effects models. The influence of the frequency of aspirin use, duration of aspirin use, and geographic location on gastric cancer incidence was evaluated. Results The meta‐analysis comprised 33 studies with a total of 1 927 971 patients. The pooled risk ratios for gastric cancer incidence in the fixed‐ and random‐effects models were 0.890 (95% confidence interval, 0.871–0.909) and 0.826 (0.740–0.922), respectively. In Asia and North America, the maximum preventive benefit of aspirin use was observed with weekly or daily use. Aspirin use was most effective for noncardiac gastric cancer. The pooled risk ratios for gastric cancer death in the fixed‐ and random‐effects models were 0.798 (0.749–0.850) and 0.894 (0.780–1.024), respectively. Significant heterogeneity was observed among studies of gastric cancer incidence but not gastric cancer death. Conclusion Aspirin use may reduce the risk of gastric cancer incidence and death; however, the relationship may be limited to a specific frequency and duration of aspirin use and geographic location.

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“…Gastric cancer is a systemic disease, and its recurrence and metastasis are the major causes of poor prognosis (4). Similar to other solid tumors, the proliferation and metastasis of gastric cancer cells are regulated by multiple genes and multiple factors (22,23). miRNA has powerful post-transcriptional regulation function and a wide application prospect in tumor therapy.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑214 promotes the proliferation, migration and invasion of gastric cancer MKN28 cells by suppressing the expression of Dact2

Zhao

Fan

et al. 2018

Exp Ther Med

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The present study examined the expression of Dapper, antagonist of β-catenin 2 (Dact2) and microRNA (miR)-214 in gastric cancer at tissue and cellular levels, and to understand their biological roles. A total of 42 gastric cancer patients were enrolled in the present study. Bioinformatics tool was used to predict the miR molecule that potentially regulates Dact2 expression. To measure the expression of miR-214 and Dact2, reverse transcription-quantitative polymerase chain reaction was employed. Mixed gastric adenocarcinoma type MKN28 cells were transfected with negative control (NC), miR-214 mimics or inhibitor. The CCK-8 assay was used to investigate the proliferation of mixed gastric adenocarcinoma type MKN28 cells. To study migration and invasion abilities of mixed gastric adenocarcinoma type MKN28 cells, the Transwell assay was performed. To determine the expression of Dact2 protein, western blotting was conducted and the rescue assay was utilized to study the biological roles of miR-214 and Dact2 in mixed gastric adenocarcinoma type MKN28 cells. To test whether Dact2 is a direct target of miR-214, the dual luciferase reporter assay was performed. Results indicated that the expression of miR-214 was elevated, but expression of Dact2 mRNA was decreased in gastric cancer tissues, which was closely correlated with the invasion, metastasis, occurrence and development of gastric cancer. Notably, miR-214 promoted the proliferation of mixed gastric adenocarcinoma type MKN28 cells in vitro, whereas but Dact2 inhibited the proliferation of these cells. Downregulation of miR-214 expression or upregulation of Dact2 expression inhibited the migration and invasion of mixed gastric adenocarcinoma type MKN28 cells. Furthermore, miR-214 regulated the expression of Dact2 protein and its downstream β-catenin protein in mixed gastric adenocarcinoma type MKN28 cells. Dact2 reversed the effect of miR-214 on the proliferation, migration and invasion of mixed gastric adenocarcinoma type MKN28 cells. In addition, miR-214 directly targeted the 3'-UTR seeding region of Dact2 mRNA to regulate its expression. The present study demonstrated that expression of miR-214 was upregulated in gastric cancer tissues, and positively correlated with lymphatic metastasis and clinical staging. In addition, expression of Dact2 was downregulated in gastric cancer tissues and negatively correlated with lymphatic metastasis and clinical staging. Notably, the present findings suggest that miR-214 promoted the proliferation, migration and invasion of mixed gastric adenocarcinoma type MKN28 cells by suppressing the expression of Dact2.

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The Origins of Gastric Cancer From Gastric Stem Cells: Lessons From Mouse Models

Cited by 55 publications

References 103 publications

YAP/TAZ Initiates Gastric Tumorigenesis via Upregulation of MYC

YAP/TAZ Initiates Gastric Tumorigenesis via Upregulation of MYC

Effect of aspirin use on gastric cancer incidence and survival: A systematic review and meta‐analysis

MicroRNA‑214 promotes the proliferation, migration and invasion of gastric cancer MKN28 cells by suppressing the expression of Dact2

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