ZNF143 enhances metastasis of gastric cancer by promoting the process of EMT through PI3K/AKT signaling pathway.

The zinc finger protein 143 (ZNF143) is a transcription factor, which regulates many cell cycle-associated genes. ZNF143 expressed strongly in multiple solid tumors. However, the influence of ZNF143 on gastric cancer (GC) remains largely unknown. 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. 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. It is conceivable that ZNF143 could be a therapeutic genetic target for GC treatment.