Bacterial Involvement in Progression and Metastasis of Adenocarcinoma of the Stomach

Abstract

Gastric cancer metastasis is a process in which the tumor microenvironment may carry significant influence. Helicobacter pylori (H. pylori) infection is well-established as a contributor to gastric carcinoma. However, the role that these bacteria and others may play in gastric carcinoma metastasis is a current focus of study. A review of the literature was conducted to elucidate the process by which gastric adenocarcinoma metastasizes, including its ability to utilize both the lymphatic system and the venous system to disseminate. Studies that investigate the tumor microenvironment at both the primary and secondary sites were assessed in detail. H. pylori and Mycoplasma hyorhinis (M. hyorhinis) were found to be important drivers of the pathogenesis of gastric adenocarcinoma by modifying various steps in cell metastasis, including epithelial–mesenchymal transition, cell migration, and cell invasion. H. pylori is also a known driver of MALT lymphoma, which is often reversible simply with the eradication of infection. M. hyorhinis has been implicated in gastric neoplasia via β-catenin stabilization and subsequent activation of the WNT-signaling pathway, promoting gastric cancer cell motility and inciting cancer progression. Fusobacterium nucleatum (F. nucleatum) and its association with worse prognosis in diffuse-type gastric adenocarcinoma are also reviewed. Recognition of the roles that bacteria play within the metastatic cascade is vital in gastrointestinal adenocarcinoma treatment and potential reoccurrence. Further investigation is needed to establish potential treatment for metastatic gastric carcinoma by targeting the tumor microenvironment.

Hp0521 inhibited the virulence of H. pylori 26,695 strain via regulating CagA expression

“…Gastric cancer is the fifth most common malignancy and the third leading cause of cancer death . H. pylori has been confirmed as the grade I carcinogen and the only pathogen to be capable of being planted in the human stomach [ 30 ], which led to immune activation and chronic inflammatory reaction [ 31 , 32 ]. Epidemiological studies showed that the global infection rate of H. pylori was about 50% [ 32 , 33 ].10–15% of infected people develop ulcers, nearly 1% develop gastric cancer and almost 90% non-cardia gastric cancer are attributed to this bacterial infection [ 32 , [34] , [35] , [36] ].…”

Small Extracellular Vesicles Derived from Helicobacter Pylori‐Infected Gastric Cancer Cells Induce Lymphangiogenesis and Lymphatic Remodeling via Transfer of miR‐1246

“…[ 4 ] Moreover, H. pylori is positively associated with GC‐LNM and poor prognosis. [ 5,6 ] In this study, we attempted to determine whether H. pylori infection promotes LNM in patients with GC and explore the underlying regulatory mechanisms.…”