title: Helicobacter pylori-infected MSCs acquire a pro-inflammatory phenotype and induce human gastric cancer migration by promoting EMT in gastric cancer cells.
abstract: Accumulating clinical and experimental evidence has suggested thatHelicobacter pylori(H. pylori) infection-associated gastric cancer (GC) is associated with high rates of mortality and serious health effects. The majority of patients succumb toH. pyloriinfection-associated GC due to metastasis. Mesenchymal stem cells (MSCs), which have multipotent differentiation potential, may be recruited into the tumor-associated stroma. MSCs are crucial components of theH. pyloriinfection-associated GC microenvironment, and may be critical for GC cell migration. In this study, an MSCs/H. pylorico-culture model was designed, and the effect ofH. pylori-infected MSCs on the migration of GC cells was evaluated using a Transwell migration assay.H. pylori-infected MSC cytokine expression was evaluated using Luminex/ELISA. The expression of epithelial-mesenchymal transition (EMT) markers in the GC cells treated with supernatants fromH. pylori-infected MSCs were detected by western blot analysis. The results demonstrated that the interaction between MSCs andH. pylorimay induce GC cell migration, through secretion of a combination of cytokines that promote EMT in GC cells. The expression of phosphorylated forms of nuclear factor-κB (NF-κB) was observed to be increased in MSCs byH. pylori. Inhibition of NF-κB activation by pyrrolidine dithiocarbamate blocked the effects ofH. pylori-infected MSCs on SGC-7901 human stomach adenocarcinoma cell migration. Overall, the results of the present study suggest thatH. pylori-infected MSCs acquire a pro-inflammatory phenotype through secretion of a combination of multiple cytokines, a number of which are NF-κB-dependent. These cytokines enhanceH. pyloriinfection-associated GC cell migration by promoting EMT in GC cells. The results of the present study provide novel evidence for the modulatory effect of MSCs in the tumor microenvironment and provide insight into the significance of stromal cell involvement in GC progression.
authors: Department of Clinical Laboratory Science, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233004, P.R. China.
authors: Qiang
authors: Q
authors: Zhang
authors: Department of Clinical Laboratory Science, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233004, P.R. China; Department of Clinical Laboratory, Bengbu Medical College, Bengbu, Anhui 233030, P.R. China.
authors: Juan
authors: J
authors: Ding
authors: Department of Clinical Laboratory Science, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233004, P.R. China.
authors: Jinjun
authors: J
authors: Liu
authors: Department of Clinical Laboratory Science, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233004, P.R. China.
authors: Wei
authors: W
authors: Wang
authors: Department of Clinical Laboratory Science, The First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233004, P.R. China.
authors: Feng
authors: F
authors: Zhang
authors: Department of Clinical Laboratory, Bengbu Medical College, Bengbu, Anhui 233030, P.R. China.
authors: Junhe
authors: J
authors: Wang
authors: Department of Clinical Laboratory, Bengbu Medical College, Bengbu, Anhui 233030, P.R. China.
authors: Yuyun
authors: Y
authors: Li
keywords: Helicobacter pylori; epithelial-mesenchymal transition; gastric cancer; mesenchymal stem cells; migration