GATA3 acetylation at K119 by CBP inhibits cell migration and invasion in lung adenocarcinoma

GATA3 is a transcriptional factor involved in the development of multiple organs. Post translational modifications of GATA3 are critical to its function. Here, we report that GATA3 interacts with and is acetylated by the acetyltransferase CBP. Class I deacetylases HDAC1, HDAC2 and HDAC3 deacetylate GATA3. The major acetylated site of GATA3 in lung adenocarcinoma cells was determined at lysine 119 (AcK119). Functionally, GATA3-acetylation mimics K119Q mutant was found to inhibit lung adenocarcinoma cell migration and invasion with concomitant downregulation of EMT-controlling transcriptional factors Slug, Zeb1 and Zeb2. Taken together, we demonstrated that GATA3 acetylation at lysine 119 by CBP hinders the migration and invasion of lung adenocarcinoma cells. •GATA3 interacts with and is acetylated by the acetyltransferase CBP.•The major acetylated site of GATA3 in lung adenocarcinoma cells is lysine 119.•GATA3 is deacetylated by Class I deacetylases HDAC1, HDAC2 and HDAC3.•The acetylation status of GATA3-K119 is critical to lung adenocarcinoma progression.