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Background  Gastric cancer is one of the most common and lethal type of cancer worldwide. Infection with  Helicobacter pylori  ( H. pylori ) is recognized as the major cause of gastric cancer. However, it remains unclear the mechanism by which  Helicobacter  infection leads to gastric cancer. Furthermore, the underlying molecular events involved during the progression of  Helicobacter  infection to gastric malignancy are not well understood. In previous studies, we demonstrated that that  H. felis -infected  Myd88   −/−  mice exhibited dramatic pathology and an accelerated progression to gastric dysplasia; however, the MyD88 downstream gene targets responsible for this pathology have not been described. This study was designed to identify MyD88-dependent genes involved in the progression towards gastric cancer during the course of  Helicobacter  infection.    Methods  Wild type (WT) and  Myd88  deficient mice ( Myd88   −/− ) were infected with  H. felis  for 25 and 47 weeks and global transcriptome analysis performed on gastric tissue using MouseWG-6 v2 expression BeadChips microarrays. Function and pathway enrichment analyses of statistically significant, differential expressed genes ( p  < 0.05) were performed using the Database for Annotation, Visualization and Integrated Discovery (DAVID) online tools.    Results    Helicobacter  infection affected the transcriptional profile of more genes in  Myd88    −/−   mice compared to WT mice. Infection of  Myd88    −/−   mice resulted in the differential expression of 1,989 genes at 25 weeks (1031 up and 958 downregulated). At 47 weeks post- H.felis  infection, 2,162 (1140 up and 1022 downregulated) were differentially expressed. The most significant differentially upregulated gene during  Helicobacter  infection in  Myd88    −/−   mice was chitinase-like 4 (chil4), which is involved in tissue remodeling and wound healing. Other highly upregulated genes in  H. felis -infected  Myd88   −/−  mice included, Indoleamine 2,3-Dioxygenase 1 (Ido1), Guanylate binding protein 2 (Gbp2), ubiquitin D (Ubd), β  2  -Microglobulin (B2m), CD74 antigen (Cd74), which have been reported to promote cancer progression by enhancing angiogenesis, proliferation, migration, metastasis, invasion, and tumorigenecity. For downregulated genes, the highly expressed genes included, ATPase H+/K+ transporting, alpha subunit (Atp4a), Atp4b, Mucin 5 AC (Muc5ac), Apolipoprotein A-1 (Apoa1), and gastric intrinsic factor (Gif), whose optimal function is important in maintaining gastric hemostasis and lower expression has been associated with increased risk of gastric carcinogenesis.    Conclusions  These results provide a global transcriptional gene profile during the development and progression of  Helicobacter -induced gastric cancer. The data show that our mouse model system is useful for identifying genes involved in gastric cancer progression.    Electronic supplementary material  The online version of this article (doi:10.1186/s12885-017-3114-y) contains supplementary material, which is available to authorized users.

bmc cancer

Effect of myeloid differentiation primary response gene 88 on expression profiles of genes during the development and progression of Helicobacter-induced gastric cancer