Autophagy was originally viewed as a widely conserved multistep lysosomal degradation pathway in eukaryotes. It includes the formation of autophagosomes, doublemembrane structures engulfing cytoplasm with damaged organelles during the degradation process.

β-Catenin is the central modulator of the canonical Wnt signaling pathway. Upon Wnt on state, β-Catenin is translocated to the nucleus and function as a transcription coactivator for several oncogenes. In Wnt off state, β-catenin is mostly localized in the cytoplasm and sequestered by the destruction complex, the negative regulator of β-catenin expression [2,3].

DIS3L2 is a 3’-5’ exoribonuclease that recognizes and degrades uridylated transcripts in an exosome-independent manner and participates in several RNA degradation pathways, such as the nonsense-mediated mRNA decay, or the surveillance of aberrant structured non-coding RNAs. Although some studies have linked DIS3L2 to tumorigenesis and cancer-related processes, its exact role in the development and progression of cancer

The Activating Molecule in Beclin-1-Regulated Autophagy (AMBRA1) is a scaffold protein involved in many cellular processes, including autophagy, apoptosis, cell growth and development. AMBRA1 functions as a substrate receptor of the DDB1-Cullin4-RBX1 ubiquitin E3 ligase complex that plays key roles in autophagy and the cell cycle regulatory network. Considering the crucial role of AMBRA1 in cellular homeostasis, structural and functional studies are important for understanding the mechanisms that coordinate these cell responses.