ZNF460 mediates epithelial-mesenchymal transition to promote gastric cancer progression by transactivating APOC1 expression

Zinc finger protein 460 (ZNF460) is closely related to the progression of a variety of human cancers. However, the biological role of ZNF460 in gastric cancer remains fully unrevealed. This study aimed to investigate the role and potential mechanism of ZNF460 in gastric cancer. In this study, we discovered a significant up-regulation of ZNF460 in gastric cancer and that ZNF460 expression correlated with tumor grade, lymph node metastasis, and H. pylon infection in gastric cancer through UALCAN database. Functionally, Diminished ZNF460 expression inhibited gastric cancer cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in vitro and suppressed tumor growth in vivo. Mechanistically, ZNF460 combined with apolipoprotein C1 (APOC1) promoter to facilitate APOC1 transcription, and accelerated EMT, thereby promoting the progression of gastric cancer. In conclusion, our study confirmed that ZNF460 promotes gastric cancer progression, which might serve as a novel target for gastric cancer treatment.

Automated summary

This study revealed the significant up-regulation of ZNF460 in gastric cancer, and its expression correlated with tumor grade, lymph node metastasis, and H. pylori infection. Functionally, diminished ZNF460 expression inhibited gastric cancer cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in vitro, and suppressed tumor growth in vivo. Mechanistically, ZNF460 combined with apolipoprotein C1 (APOC1) promoter to facilitate APOC1 transcription and accelerated EMT, thereby promoting gastric cancer progression.