HGF-mediated S100A11 overexpression enhances proliferation and invasion of gastric cancer.

Abstract

invasion increased, and HGF-mediated apoptosis decreased in S100A11 knockdown cells. We identified the putative binding site of NF-κB in the MMP9 promoter region and confirmed its function via chromatin immunoprecipitation (CHIP) assay. Our results showed that S100A11 is upregulated by HGF through the NF-κB pathway in gastric cancer and plays a role in cell proliferation and invasion in gastric cancer. It may thus be a possible target for gastric cancer therapy.