Mechanistically, the AR suppressed the RNA-editing gene ADAR2 by binding to the promoter region to increase circFNTA levels, which then sponged miR-370-3p to upregulate the expression of its host gene FNTA. This AR-mediated ADAR2/circFNTA/miR-370-3p/FNTA axis subsequently activated KRAS signaling to dysregulate cancer invasion and promote chemoresistance to cisplatin. Here, FNTA is linked to cancer.