Knockdown of HMGB1 inhibits growth and invasion of gastric cancer cells through the NF-κB pathway in vitro and in vivo

摘要: High mobility group box 1 (HMGB1) as a novel inflammatory molecule has been shown to be involved in variety of cell physiological and pathological behaviors including immune response, inflammation cancer. Evidence suggests that HMGB1 plays critical role the development progression multiple malignancies. However, underlying molecular mechanisms for HMGB1-mediated growth invasion gastric cancer have not yet elucidated. The present study investigated expression adenocarcinoma (GAC) by which it contributes tumor invasion. correlation between clinicopathological characteristics GAC patients was assessed immunohistochemical assay through tissue microarray procedures. RNA protein expressions downstream factors were detected quantitative PCR western blot assays; proliferation determined MTT, wound-healing 3D-Matregel assays, subcutaneous SGC-7901 models established verify vivo. We demonstrated that, significantly increased nucleus tissues compared with adjacent non-cancer (88.6 vs.70.5%, P<0.001), correlated metastatic lymph node (P=0.018). Furthermore, knockdown shRNA inhibited proliferative activities invasive potential, downregulated NF-κB p65, PCNA MMP-9 cells (SGC-7901 AGS). volumes SGC7901 nude mouse treated Lv-shHMGB1 smaller than those nonsense sequence group. Taken together, these findings suggest is associated metastasis GAC, suppresses pathway vitro vivo, suggesting may serve potential therapeutic target GAC.