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

This study aimed to identify the function of S100A11 associated with cell proliferation and invasion in gastric cancer. We used cell culture, western blotting, reverse transcription-polymerase chain reaction, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, and S100A11 knock-down with short hairpin ribonucleic acid (shRNA). First, we confirmed that the S100A11 expression was upregulated by hepatocyte growth factor (HGF). The role of S100A11 was determined via knock down of S100A11. S100A11-shRNA cells showed decreased levels of metalloproteinase-9 (MMP9) and nuclear factor kappa-B (NF-κB). We also examined and confirmed the role of HGF-mediated S100A11 expression. HGF-mediated cell proliferation and in vitro 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. PMID: 30662594 [PubMed]
Source: American Journal of Translational Research - Category: Research Tags: Am J Transl Res Source Type: research