Helicobacter pylori infection induces stem cell-like properties in Correa cascade of gastric cancer. (28th August 2022)
- Record Type:
- Journal Article
- Title:
- Helicobacter pylori infection induces stem cell-like properties in Correa cascade of gastric cancer. (28th August 2022)
- Main Title:
- Helicobacter pylori infection induces stem cell-like properties in Correa cascade of gastric cancer
- Authors:
- He, JunJian
Hu, WeiChao
Ouyang, Qin
Zhang, ShengWei
He, LiJiao
Chen, WeiYan
Li, XinZhe
Hu, ChangJiang - Abstract:
- Abstract: Gastric cancer (GC) is the fourth leading cause of cancer-related death. Its poor prognosis is attributed to unclear pathogenesis. Currently, the most widely accepted model for elucidating the mechanism of GC is the Correa cascade, which covers several histological lesions of the gastric mucosa. GC stem cells (CSCs) are crucial for oncogenesis in the Correa cascade and GC progression. As Helicobacter pylori ( H. pylori ) is the etiological factor in the Correa cascade, growing evidence suggests that enhancement of gastric stem cell-like properties and increase in CSCs correlate with H. pylori infection. In this paper, we review recent studies that present pathogenic mechanisms by which H. pylori induces gastric stem cell-like properties and CSCs, which may supplement the existing Correa model of GC. First, the dysfunction of developmental signaling pathways associated with H. pylori infection leads to the enhancement of gastric stemness. Second, H. pylori infection promotes alteration of the gastric mucosal microenvironment. In addition, epithelial–mesenchymal transition (EMT) may contribute to H. pylori- induced gastric stemness. Taken together, understanding these pathogeneses will provide potential therapeutic targets for the treatment of CSCs and malignant GC in H. pylori induced-Correa cascade of GC. Highlights: H. pylori infection induced gastric stem cell-like properties in Correa cascade progression based on epidemiological investigation and basic research.Abstract: Gastric cancer (GC) is the fourth leading cause of cancer-related death. Its poor prognosis is attributed to unclear pathogenesis. Currently, the most widely accepted model for elucidating the mechanism of GC is the Correa cascade, which covers several histological lesions of the gastric mucosa. GC stem cells (CSCs) are crucial for oncogenesis in the Correa cascade and GC progression. As Helicobacter pylori ( H. pylori ) is the etiological factor in the Correa cascade, growing evidence suggests that enhancement of gastric stem cell-like properties and increase in CSCs correlate with H. pylori infection. In this paper, we review recent studies that present pathogenic mechanisms by which H. pylori induces gastric stem cell-like properties and CSCs, which may supplement the existing Correa model of GC. First, the dysfunction of developmental signaling pathways associated with H. pylori infection leads to the enhancement of gastric stemness. Second, H. pylori infection promotes alteration of the gastric mucosal microenvironment. In addition, epithelial–mesenchymal transition (EMT) may contribute to H. pylori- induced gastric stemness. Taken together, understanding these pathogeneses will provide potential therapeutic targets for the treatment of CSCs and malignant GC in H. pylori induced-Correa cascade of GC. Highlights: H. pylori infection induced gastric stem cell-like properties in Correa cascade progression based on epidemiological investigation and basic research. Specific activation of signal transduction cascades facilitated the stemness of gastric mucosa. Altered-gastric mucosal microenvironment enhanced the stem cell characteristics. … (more)
- Is Part Of:
- Cancer letters. Volume 542(2022)
- Journal:
- Cancer letters
- Issue:
- Volume 542(2022)
- Issue Display:
- Volume 542, Issue 2022 (2022)
- Year:
- 2022
- Volume:
- 542
- Issue:
- 2022
- Issue Sort Value:
- 2022-0542-2022-0000
- Page Start:
- Page End:
- Publication Date:
- 2022-08-28
- Subjects:
- Cancer stem cell -- Microenvironment remodeling -- Epithelial–mesenchymal transition
Cancer -- Periodicals
Neoplasms -- Periodicals
Cancer -- Périodiques
Electronic journals
616.994 - Journal URLs:
- http://www.sciencedirect.com/science/journal/03043835/ ↗
http://www.elsevier.com/journals ↗ - DOI:
- 10.1016/j.canlet.2022.215764 ↗
- Languages:
- English
- ISSNs:
- 0304-3835
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 3046.485000
British Library DSC - BLDSS-3PM
British Library HMNTS - ELD Digital store - Ingest File:
- 21800.xml