Notch as a Driver of Gastric Epithelial Cell ProliferationSummary
The gastric epithelium is sustained by a population of stem cells that replenish the various mature epithelial lineages throughout adulthood. Regulation of stem and progenitor cell proliferation occurs via basic developmental signaling pathways, including the Notch pathway, which recently was descri...
| Main Authors: | , |
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| Format: | Article |
| Language: | English |
| Published: |
Elsevier
2017-05-01
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| Series: | Cellular and Molecular Gastroenterology and Hepatology |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2352345X17300292 |
| _version_ | 1811314482597593088 |
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| author | Elise S. Demitrack Linda C. Samuelson |
| author_facet | Elise S. Demitrack Linda C. Samuelson |
| author_sort | Elise S. Demitrack |
| collection | DOAJ |
| description | The gastric epithelium is sustained by a population of stem cells that replenish the various mature epithelial lineages throughout adulthood. Regulation of stem and progenitor cell proliferation occurs via basic developmental signaling pathways, including the Notch pathway, which recently was described to promote gastric stem cell proliferation in both mice and human beings. Current cancer theory proposes that adult stem cells that maintain gastrointestinal tissues accumulate mutations that promote cancerous growth, and that basic signaling pathways, such as Notch, which stimulate stem cell proliferation, can promote tumorigenesis. Accordingly, constitutive Notch activation leads to unchecked cellular proliferation and gastric tumors in genetic mouse models. Furthermore, there is emerging evidence suggesting that the Notch pathway may be activated in some human gastric cancers, supporting a potential role for Notch in gastric tumorigenesis. In this review, we first summarize the current understanding of gastric stem cells defined by genetic mouse studies, followed by discussion of the literature regarding Notch pathway regulation of gastric stem cell function in the mouse and human beings. Notch action to maintain gastric epithelial cell homeostasis and the cellular consequences of dysregulated signaling to promote tumorigenesis are discussed, including studies associating Notch activation with human gastric cancer. Finally, we compare and contrast Notch function in the stomach with other gastrointestinal tissues, including the intestine, to highlight the sensitivity of the stomach to Notch-induced tumors. Keywords: Stomach, Homeostasis, Gastric Stem Cells, Gastric Cancer |
| first_indexed | 2024-04-13T11:13:30Z |
| format | Article |
| id | doaj.art-90ccb8081d454f1cb67234c06b824564 |
| institution | Directory Open Access Journal |
| issn | 2352-345X |
| language | English |
| last_indexed | 2024-04-13T11:13:30Z |
| publishDate | 2017-05-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Cellular and Molecular Gastroenterology and Hepatology |
| spelling | doaj.art-90ccb8081d454f1cb67234c06b8245642022-12-22T02:49:03ZengElsevierCellular and Molecular Gastroenterology and Hepatology2352-345X2017-05-0133323330Notch as a Driver of Gastric Epithelial Cell ProliferationSummaryElise S. Demitrack0Linda C. Samuelson1Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MichiganDepartment of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, Michigan; Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan; Correspondence Address correspondence to: Linda C. Samuelson, PhD, Department of Molecular and Integrative Physiology, University of Michigan, 109 Zina Pitcher Place, 2041 BSRB, Ann Arbor, Michigan 48109.The gastric epithelium is sustained by a population of stem cells that replenish the various mature epithelial lineages throughout adulthood. Regulation of stem and progenitor cell proliferation occurs via basic developmental signaling pathways, including the Notch pathway, which recently was described to promote gastric stem cell proliferation in both mice and human beings. Current cancer theory proposes that adult stem cells that maintain gastrointestinal tissues accumulate mutations that promote cancerous growth, and that basic signaling pathways, such as Notch, which stimulate stem cell proliferation, can promote tumorigenesis. Accordingly, constitutive Notch activation leads to unchecked cellular proliferation and gastric tumors in genetic mouse models. Furthermore, there is emerging evidence suggesting that the Notch pathway may be activated in some human gastric cancers, supporting a potential role for Notch in gastric tumorigenesis. In this review, we first summarize the current understanding of gastric stem cells defined by genetic mouse studies, followed by discussion of the literature regarding Notch pathway regulation of gastric stem cell function in the mouse and human beings. Notch action to maintain gastric epithelial cell homeostasis and the cellular consequences of dysregulated signaling to promote tumorigenesis are discussed, including studies associating Notch activation with human gastric cancer. Finally, we compare and contrast Notch function in the stomach with other gastrointestinal tissues, including the intestine, to highlight the sensitivity of the stomach to Notch-induced tumors. Keywords: Stomach, Homeostasis, Gastric Stem Cells, Gastric Cancerhttp://www.sciencedirect.com/science/article/pii/S2352345X17300292 |
| spellingShingle | Elise S. Demitrack Linda C. Samuelson Notch as a Driver of Gastric Epithelial Cell ProliferationSummary Cellular and Molecular Gastroenterology and Hepatology |
| title | Notch as a Driver of Gastric Epithelial Cell ProliferationSummary |
| title_full | Notch as a Driver of Gastric Epithelial Cell ProliferationSummary |
| title_fullStr | Notch as a Driver of Gastric Epithelial Cell ProliferationSummary |
| title_full_unstemmed | Notch as a Driver of Gastric Epithelial Cell ProliferationSummary |
| title_short | Notch as a Driver of Gastric Epithelial Cell ProliferationSummary |
| title_sort | notch as a driver of gastric epithelial cell proliferationsummary |
| url | http://www.sciencedirect.com/science/article/pii/S2352345X17300292 |
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