regulates migration, invasion and apoptosis in cadmium transformed 16HBE cells and is a novel biomarker of cadmium exposure in a rat model and in workers.

Translation (eukaryotic) initiation factor 3 ( or ) has been found to be a proto-oncogene in cadmium (Cd) response both and , but whether may serve as a biomarker of Cd exposure is still unclear. This study aimed to investigate whether could serve as a novel biomarker of Cd toxicity in cells, animals and workers, and regulate the apoptosis, migration and invasion in human bronchial epithelial cell (16HBE cells) transformation with cadmium chloride (CdCl). In CdCl transformed 16HBE cells, expression increased gradually, and sequencing did not identify mutation and methylation of . In 16HBE cells with silencing by siRNA and CdCl treated 16HBE cells of the 15 and 35 generations, the apoptosis, migration and invasion were significantly inhibited, and the expressions of relevant genes were also altered ( < 0.05). In CdCl treated rats, mRNA expression increased to different extents in the blood, liver, kidney, heart and lung, and this increase was dependent on the Cd concentration ( < 0.05). The mRNA expression was related to the mRNA expressions of , , , , , , , , and ( < 0.05). In 181 workers with Cd exposure, the mRNA expression was positively related to the blood Cd, urine Cd and -microglobulin content ( < 0.05). This study showed that abnormally expressed may regulate the apoptosis, migration and invasion of 16HBE cells with Cd toxicity. This suggests that may become a novel and valuable biomarker of Cd toxicity and Cd-induced effects, and may regulate apoptosis, migration and invasion of 16HBE cells. Thus, the detection of expression is important for the monitoring of Cd toxicity in humans.