H. pylori - Ace Infectious
Gene Editing of Gastric Cells and Experimental Animals
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Gene Editing of Gastric Cells and Experimental Animals

Ace Infectious provides gene-editing services for gastric cells and experimental animals. This service is mainly designed for the study of H. pylori infection mechanisms.

Molecular pathogenesis of H. pylori in gastric carcinogenesis.Fig. 1 Molecular pathogenesis of H. pylori in gastric carcinogenesis (Yanan et al., 2020).

Construction of gene-edited gastric cells

Experiments using co-cultures of gastric cells and H. pylori can provide insight into the mechanisms of gastric cell adaptation triggered by H. pylori infection. These adaptive mechanisms may be exploited as pharmacological targets and are important for the development of new therapeutic approaches for non-invasive risk control of gastric diseases caused by H. pylori. Further, experiments using specially gene-edited gastric cells co-cultured with H. pylori can investigate these mechanisms in greater depth. To better assist in the study of the mechanisms of H. pylori infection in humans and to understand the interplay between H. pylori and gastric cells (especially GES-1), Ace Infectious provides specialized gastric cell gene editing services, including gene knockdown, gene overexpression and gene knockout of specific genes in gastric cells.

Let us present our service using an example of the study of Krüppel-like factor 4 (KLF4)-related mechanisms. TKLF4 is expressed in gastric terminally differentiated epithelial cells which can regulate cell differentiation and apoptosis. In gastric cancer, KLF4 is inactivated due to gene promoter methylation. Previous studies found that KLF4 protein expression was decreased in both GES-1 and AGS cells transfected with the H. pylori cagA gene. And the expression of TET1 was significantly down-regulated in both gastric cells. To further investigate the mechanism, we can provide four gastric cell genetic manipulation services to help study the H. pylori/CagA-TET1-KLF4 relationship.

  1. Overexpress both KLF4 gene and TET1 gene in gastric cells
  2. Simultaneous knockout or knockdown of KLF4 and TET1 genes in gastric cells
  3. Overexpression of KLF4 gene or TET1 gene in gastric cells
  4. Knockdown or knockdown of KLF4 or TET1 gene in gastric cells

Construction of gene-edited animals

Animal models of H. pylori-induced gastric cancer (GC) can be used to study the interaction between host and H. pylori and elucidate the mechanisms of H. pylori-induced GC in humans. However, a deeper understanding of the mechanism of H. pylori-induced GC in humans requires the power of gene editing. Therefore, Ace Infectious provides experimental animal gene-editing services to facilitate the exploration of H. pylori-induced GC and other gastric disease mechanisms. We focus on gene editing in rodent models because the pathological processes in the stomach of rodent models caused by H. pylori are very similar to those in the human stomach.

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It is well known that at least 90% of gastric cancers are related to H. pylori. And it is important to study the reaction between H. pylori and gastric diseases for the prevention and therapy of H. pylori-related gastric diseases. If you need gene-edited gastric cells or experimental animals to study the mechanisms of H. pylori infection, please contact us without hesitation.

References

  1. Zhao, Y.; et al. Gastric cancer: genome damaged by bugs. Oncogene. 2020, 39: 1-16.
  2. Zhao, R.; et al. Helicobacter pylori infection leads to KLF4 inactivation in gastric cancer through a TET1-mediated DNA methylation mechanism. Cancer Medicine. 2020, 9(7): 2551-63.
  3. Peng, C.; et al. Impact factors that modulate gastric cancer risk in Helicobacter pylori-infected rodent models. Helicobacter. 2019, 24(4): e12580.

※ All of our services and products are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.