In conclusion, our results suggest that ISL has potential for development as a chemosensitizing agent for breast cancer due to its ability to inhibit miR-25 expression, which in turn leads to the upregulation of its target gene ULK1 and the induction of autophagic cell death, ultimately resulting in accelerated ABCG2 degradation via the lysosome pathway. This evidence concerns the gene ABCG2 and breast carcinoma.