GATAD2A (GATA zinc finger domain containing 2A), is a subunit of NuRP (nucleosome remodeling and histone deacetylation) which plays key roles in tumor growth inhibition and embryonic development. However, its role in thyroid cancer remains unclear. In our study, we established two thyroid cancer cell lines by lentivirus-delivered short hairpin (shRNA) to knockdown the expression of GATAD2A. Then loss-of-function assays indicated that knockdown of GATAD2A decreased the ability of cell proliferation and colony formation in thyroid cancer cells by MTT and colony formation assay, respectively. Moreover, cell cycle assay by flow cytometry revealed that the percentage of cells in G0/G1 phase was significantly decreased in GATAD2A knockdown cells accompanied by increase of cells in G2/M phase. Furthermore, inhibition of GATAD2A promoted cell apoptosis via elevating the expression of caspase-3 and PARP cleavage using Annexin V/7-AAD double staining and western blotting. In conclusion, GATAD2A is an essential factor in thyroid cancer cell growth and apoptosis, and may be a potential therapeutic biomarker in thyroid cancer.