Abstract
GATA3, a member of the GATA zinc finger transcription factor family, has been widely investigated for its role in cancer. Although a recent report has found that GATA3 is downregulated in gastric cancer (GC), the detailed mechanism of GATA3 in GC is still unknown. Here, we investigated whether GATA3 was downregulated in GC patients' tissue samples and cell lines using quantitative real time polymerase chain reaction and Western blotting. In addition, we conducted several functional experiments to investigate the effect of GATA3 in GC, including cell proliferation, metastasis and epithelial-mesenchymal transition (EMT). The results showed that GATA3 was downregulated in GC tissue samples and cells. Moreover, the expression of GATA3 was associated with tumor size, stage and metastasis. Restoration of GATA3 levels suppressed GC cell proliferation, migration and invasion. Furthermore, chromatin immunoprecipitation and luciferase reporter assay also revealed that GATA3 transcriptionally regulated ZEB1, thereby suppressing EMT. All these findings suggest that GATA3 serves as an oncogene in GC development.