Abstract
BackgroundGastric cancer is one of the most common and lethal malignant cancers worldwide, and numerous epidemiological studies have demonstrated that Helicobacter pylori (H. pylori) infection plays a key role in the development of gastric carcinomas. Our previous studies showed that aquaporin 3 (AQP3) is overexpressed in gastric carcinoma and promotes the migration and proliferation of human gastric carcinoma cells, suggesting that AQP3 may be a potentially important determinant of gastric carcinoma. However, the role of AQP3 in H. pylori carcinogenesis is unknown.MethodsThe AQP3 protein and H. pylori were detected in human gastric tissues by immunohistochemistry and modified Giemsa staining respectively. AQP3 knockdown was obtained by small interfering (si) RNA. Western blot assays and RT-PCR were used to evaluate the change of AQP3 in the human gastric cancer AGS and SGC7901 cell lines after co-culture with H. pylori. Sprague Dawley rats were orally inoculated with H. pylori to establish a rat model colonized by H. pylori.ResultsThe present study found that AQP3 expression correlated with H. pylori infection status in gastric cancer tissues and corresponding normal mucosa, and H. pylori co-culture upregulated AQP3 expression in human gastric adenocarcinoma cells in vitro via the extracellular signal-regulated kinase signaling pathway. H. pylori infection also increased AQP3 expression in gastric mucosa colonized by H. pylori in a Sprague Dawley rat model.ConclusionsThese findings provide further information to understand the mechanism of H. pylori carcinogenesis and a potential strategy for the treatment of H. pylori-associated gastric carcinoma.
Highlights
Gastric carcinoma remains one of the most common and lethal malignancies worldwide, with approximately 1 million cases diagnosed annually, accounting for 738,000 deaths in 2008
We showed previously that human gastric carcinoma tissues expressed higher levels of aquaporin 3 (AQP3) than normal mucosa, and AQP3 expression was associated with histological classification, lymph node metastasis, and lymphovascular invasion [18,19], suggesting that AQP3 may play an important role in human gastric cancer
We found that AQP3 expression in gastric cancer tissues correlated with H. pylori infection status, and H. pylori upregulated AQP3 expression in human gastric adenocarcinoma cells in vitro via the extracellular signal-regulated kinase (ERK) signaling pathway, confirmed by experimental gastric helicobacter infection in rats
Summary
Gastric carcinoma remains one of the most common and lethal malignancies worldwide, with approximately 1 million cases diagnosed annually, accounting for 738,000 deaths in 2008. Numerous epidemiological studies have indicated that Helicobacter pylori (H. pylori) plays a key role in the development of both intestinal-type and diffuse-type gastric carcinomas, especially in the distal portion of the stomach [2,3,4]. Recent studies showed that infection with CagA-positive H. pylori plays an essential role in the development of gastric carcinoma. H. pylori infection may cause a combination of increased endogenous DNA damage, decreased repair activity, and the induction of mutations in mitochondrial DNA that generate genetic instability in gastric cells and promote gastric carcinogenesis [14]. Gastric cancer is one of the most common and lethal malignant cancers worldwide, and numerous epidemiological studies have demonstrated that Helicobacter pylori (H. pylori) infection plays a key role in the development of gastric carcinomas. The role of AQP3 in H. pylori carcinogenesis is unknown
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