Abstract
Helicobacter pylori infection is the major cause of gastric cancer, which remains an important health care challenge. Recent investigation in gastric stem cell or progenitor cell biology has uncovered valuable information in understanding the gastric gland renewal and maintenance of homeostasis, they also provide clues for further defining the mechanisms by which gastric cancer may originate and progress. Lgr5, Villin-promoter, TFF2-mRNA and Mist have recently been identified as gastric stem/progenitor cell markers; their identification enriched our understanding on the gastric stem cell pathobiology during chronic inflammation and metaplasia. In addition, advance in gastric cancer stem cell markers such as CD44, CD90, CD133, Musashi-1 reveal novel information on tumor cell behavior and disease progression implicated for therapeutics. However, two critical questions remain to be of considerable challenges for future exploration; one is how H. pylori or chronic inflammation affects gastric stem cell or their progenitors, which give rise to mucus-, acid-, pepsinogen-, and hormone-secreting cell lineages. Another one is how bacterial infection or inflammation induces oncogenic transformation and propagates into tumors. Focus on the interactions of H. pylori with gastric stem/progenitor cells and their microenvironment will be instrumental to decipher the initiation and origin of gastric cancer. Future studies in these areas will be critical to uncover molecular mechanisms of chronic inflammation-mediated oncogenic transformation and provide options for cancer prevention and intervention. We review recent progress and discuss future research directions in these important research fields.
Highlights
Helicobacter pylori, a microaerophilic, spiral-shaped Gram-negative bacterium, colonized in human stomach, is the major cause of chronic gastritis, peptic ulcers, and gastric malignancies, including gastric non-cardia adenocarcinoma and mucosal-associated lymphoid tissue (MALT) lymphoma [1]
Blocking ERBB2 pathway can suppress tumorigenicity, and reduce tumor mass/growth when combined with traditional chemotherapy [35]. These results suggest Cluster of differentiation 90 (CD90) can be a potential cancer stem cell marker and implicated for monitoring gastric cancers treatment
CD133 is expressed in more than 50% of the cases, and its expression appears as an independent prognostic marker for poor patient prognosis, high CD133 is associated with poor patient survival rates [40]
Summary
Helicobacter pylori, a microaerophilic, spiral-shaped Gram-negative bacterium, colonized in human stomach, is the major cause of chronic gastritis, peptic ulcers, and gastric malignancies, including gastric non-cardia adenocarcinoma and mucosal-associated lymphoid tissue (MALT) lymphoma [1]. The fact that cancer formation does not require H. pylori infection indicate that the general inflammatory status, or microenvironment, not necessarily bacterial factors or components, may play a more important role in regulating stem cell differentiation and the initiation of gastric cancer; while H. pylori or H. felis components might promote this process These finding are supported by recent finding from H. pylori infected gerbil model, in which H. pylori infection induces remarkable inflammation and resulted gastric epithelial cell DNA methylation and stomach malignancy; which is caused by inflammation but not by H. pylori itself [51]. Future studies are required to define the role of H. pylori or its components in disrupting stem cell niche, their self-renewal, differentiation, and tumorigenesis
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