Fig. 4

High-dose doxorubicin activated autophagy flux in DR-BC cells through regulating AMPK-ULK1 pathway, examined by Western Blot analysis. a, b High-dose doxorubicin specifically increased the expression levels of p-AMPLK and p-ULK1 to activate AMPK-ULK1 pathway in DR-BC cells, instead of DS-BC cells. The AMPK-ULK1 pathway was successfully blocked by its inhibitor, c, d compound C and e, f SBI-0206965. g, h Blockage of AMPK-ULK1 pathway decreased LC3B-II/I ratio, and increased p62 expression levels to reverse doxorubicin induced autophagy in DR-BC cells (full-length blots/gels are presented in Supplementary Fig. S6A-H). Each experiment repeated at least 3 times, and *P < 0.05 was regarded as statistical significance