ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016
Role of Helicobacter pylori on cancer of human adipose-derived mesenchymal stem cells and metastasis of tumor cells-an in vitro study.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Mechanism of crosstalk between Helicobacter pylori and immune stromal cells in the development and occurrence of gastric cancer.Discover oncology · 2025Review
- The interplay between persistent pathogen infections with tumor microenvironment and immunotherapy in cancer.Cancer medicine · 2024Review
- Matrix Metalloproteinases inInternational journal of molecular sciences · 2022Review
- Effects ofFrontiers in immunology · 2022Review
- Sodium Selenite Regulates the Proliferation and Apoptosis of Gastric Cancer Cells by Suppressing the Expression of LncRNA HOXB-AS1.Evidence-based complementary and alternative medicine : eCAM · 2022Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have shown that Helicobacter pylori has a special role in tropism of mesenchymal stem cells (MSCs) towards gastric tissues. This study aimed to find the effects of H. pylori on human adipose-derived mesenchymal stem cells (hA-MSCs) transforming toward cancer cells and also metastasis of tumor cells by synergic effects of H. pylori and gastric epithelial cells (AGS) on MSCs. The expressions of p53, bcl-2, MMP-2, and MMP-9 were examined in hA-MSCs by qRT-PCR technique. Our results demonstrated that H. pylori tries to improve the hA-MSCs carcinogenic activities by overexpression of bcl2 gene as an anti-apoptosis agent against the p53 gene expression as main apoptosis agent. In addition, it showed that H. pylori effects in metastatic activities of hA-MSCs by upregulation of related genes in this process. Perhaps, when hA-MSCs are attracted toward H. pylori chronic or ulcer infected tissues for their tissue healing function, they will be trapped under special gastric microenvironment. We demonstrated the direct and synergic effects of H. pylori in hA-MSCs through alteration of related genes involved in carcinogenesis processes. Hence, understanding of H. pylori-induced molecular pathogenesis could be a powerful strategy not only in identifying the origin and initiation of gastric cancer but also in the treatment of related disease and modification of stem cell therapy methods in the future.
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