Helicobacter pylori-induced miR-136 is a potential predictor of early-stage gastric cancer

BACKGROUND MicroRNAs play an important role in gastric cancer (GC) development following Helicobacter pylori (H. pylori ) infection. Yet the exact mechanism is still not fully understood. Herein, we investigated the underlying mechanisms of miR-136 during this process. AIM To investigate the role of miR-136 in H. pylori -induced GC progression. METHODS GC and gastric epithelial cells were infected with H. pylori and transfected with miR-136 mimic, inhibitor, mimic plus PDCD11 (identified as miR-136 target), or miR-NC (control). Cell proliferation, migration, and invasion were assessed via cell counting kit-8 assay, colony formation, wound healing, and Transwell assays. Nuclear factor kappa-B (NF-κB)/miR-136/PDCD11 interactions were confirmed by luciferase and inhibition assays. For in vivo studies H. pylori -infected BGC-823 cells were injected into nude mice. Reverse transcription PCR, western blot, immunohistochemistry, and immunofluorescent staining assay were used to assess mRNA and protein expression. RESULTS miR-136 expression was significantly upregulated while PDCD11 expression was significantly downregulated in early GC tissues and GC cells infected with H. pylori compared with non-infected tissues or cells (all P < 0.01). miR-136 overexpression induced by H. pylori could promote the proliferation and migration of infected GC cells and induce the growth of H. pylor i-positive GC tumors in mice while its inhibition could reverse this effect. Mechanistically, upregulation of miR-136 suppressed PDCD11 through NF-κB activation induced by H. pylori infection. CONCLUSION miR-136 is a novel diagnostic biomarker and therapeutic target in H. pylori -associated early-stage gastric carcinogenesis and acts through the NF-κB-miR-136-PDCD11 pathway.