<i>H. pylori</i> infection induces CXCL8 expression and promotes gastric cancer progress through downregulating KLF4

Tumour-derived CXCL8 facilitates the movement of myeloid-derived suppressor cells, which are able to restrain antitumour immune responses tumour microenvironment. Kruppel-like factor 4 (KLF4) is a potential in gastric cancer (GC). However, knowledge regarding correlations between KLF4 and GC limited. We use cellular molecular biological methods assess whether these two factors interact GC. Expression was altered human tissues compared normal opposite ways. Additionally, cytotoxin-associated gene A protein (CagA) transduction or Helicobacter pylori (H. pylori) infection upregulated expression. Knockdown expression increased RNA expression, whereas its overexpression had effect. CXCL8-mediated enhancement cell migration proliferation reversed by upregulation Further mechanistic research revealed that binds promoter, suppressing transcription. Moreover, stimulation reduced promoted migration, eventually promoting neoplasm growth vivo. Together, our findings demonstrate CagA promotes inhibits KLF4. decisive downstream target KLF4, negatively regulates Furthermore, CXCL8's negative regulation vivo vitro, indicates may downregulate inducing low further CXCL8, forming vicious circle Targeted activation might improve immunosuppressive microenvironment through direct providing new strengthen efficacy immunotherapy patients.