| Purpose To explore the expression level of ZNF143 in gastric cancer and the association between clinical characters and the expression level of ZNF143.Methods In this study,we investigated the ZNF143 mRNA level in GC tissues and cells by quantitative real-time PCR(qRT-PCR).The protein expression of ZNF143 in GC cells and the signaling pathway proteins were detected by western blotting.Transwell assay and wound healing assay were performed to explore the effects of ZNF143 for the migration ability of GC cells in vitro.We also performed the tail vein injection in nude mice with GC cells to explore the impact of ZNF143 on GC metastasis in vivo.Results ZNF143 was overexpressed in specimens of GC compared with adjacent normal tissues and increased more significantly in GC tissues of patients who had lymph node metastasis.Ectopic overexpression of ZNF143 enhanced GC migration,whereas ZNF143 knockdown suppressed this effect in vitro.In vivo,ZNF143 knockdown reduced distant metastasis of GC cells in nude mice.In addition,overexpression of ZNF143 reduced the expression of epithelial cell marker(E-cadherin)and induced the expression of mesenchymal cell marker(N-cadherin,Vimentin),Snail and Slug.We also found that ZNF143 enhanced GC cell migration by promoting the process of EMT through PI3K/AKT signaling pathway.In general,our findings show that ZNF143 expressed strongly in GC and enhanced migration of GC cells in vitro and in vivo.Conclusions In this study,we found that high expression of ZNF143 was correlated with the lymph node metastasis in gastric cancer,indicating that ZNF143 plays an important role in metastases of gastric cancer.We also found that ZNF143 enhanced metastasis of GC cells by promoting EMT through regulating PI3K/AKT pathway.However,the underlying mechanisms for ZNF143 to promote EMT have not yet been elucidated.It still needs more attention to focus on the specific mechanism of ZNF143 to regulate the migratory of GC cells. |
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