The downregulation of CCT3 significantly inhibited the proliferation, invasion, and migration of lung adenocarcinoma cells, resulting in increased apoptosis and enhanced expression of the apoptosis marker cleaved caspase-3 (34) and leading to significant G2/M cell cycle arrest and apoptosis in lung adenocarcinoma cells, significantly reducing the tumorigenicity of cisplatin-treated lung adenocarcinoma cells. Here, CASP3 is linked to lung adenocarcinoma.