Fig. 1

AML tumorigenesis-induced fusion gene linking autophagy. ATRA increases ALFY protein-mediated autophagic degradation of the PML/RARA protein. ATRA inhibits the mTOR1 signaling pathway and then induces p62-mediated autophagic degradation of PML/RARA. The long non-coding RNA HOTAIRM1 acts as a sponge for the microRNAs, miR-20a/106b and miR-125b, targeting the genes ULK1, E2F1, and DRAM2, which are required for PML/RARA autophagic degradation. In AML with MLL/AF9 translocation, ATG5 protein-dependent autophagy aggravates the disease status. Another fusion protein, AML1-ETO, functions as an oncoprotein through ULK1-mediated autophagy; the enzyme caspase-3 destroys ULK1, inhibiting the autophagy process and tumorigenesis of AML1-ETO