English: Schematic representation of cell signaling pathways involved in autophagy and epithelial-mesenchymal-transition (EMT). 1) In the canonical WNT signaling, β-catenin stabilizes and translocates to the nucleus after binding of WNT to Frizzled and low-density lipoprotein receptor-related protein 5/6 (LRP5/6) receptors. GSK3 is sequestered together with proteins of the destruction complex of β-catenin (DVL, axin, CK1). 2) In the nucleus, β-catenin binds to TCF/LEF transcriptional factors, activating its target genes. β-catenin also stimulates transcription of important EMT transcriptional factors such as ZEB1/ZEB2, Twist and Snail/Slug. 3) EMT is also induced by the mammalian Target of Rapamycin Complex 1 (mTORC1) signaling, through activation of the transcriptional factors ZEB1/ZEB2, Twist and Snail/Slug. mTORC1 and mTORC2 are activated by tyrosine kinase receptor (TKR) signaling through PI3K/AKT. mTORC2 also stimulates AKT. 4) Depending on the energy status of the cell, activation of AMP Kinase (AMPK) inhibits mTORC1 and induces macroautophagy (MA). 5) Chaperone-mediated autophagy (CMA) degrades cytosolic proteins that possess the KFERQ or KFERQ-like motif through recognition and binding of the heat shock-cognate chaperone of 71 kDa (HSC70) and a cochaperone complex. HSC70 targets the substrate protein to the lysosomal membrane, where it binds monomeric lysosome-associated membrane protein type 2A (LAMP2A) and induces its multimerization and stabilization. The substrate protein is unfolded and translocated into the lysosome for degradation through multimerized LAMP2A. 6) In mammals, microautophagy (mA) occurs in the late endosome, in a process called endosomal microautophagy. It can degrade cytosolic proteins, and some are recognized by HSC70. Some proteins, such as GSK3, are targeted for mA through arginine methylation (meArg) by protein arginine methyltransferases (PRMTs). After entering the late endosome, this organelle fuses with lysosomes to complete the mA cycle. 7) In the noncanonical WNT signaling, WNTs bind to Frizzled receptors and DVL1 is recruited to the membrane. c-Jun N-terminal kinases (JNKs), RhoA and phosphoinositide phospholipase C (PLC) can be activated by noncanonical WNT. JNK and RhoA further regulate the cytoskeleton, and JNK induces gene transcription through activator protein 1 (AP1). PLC increases cytosolic Ca2+ levels, leading to activation of Ca2+/calmodulin-dependent protein kinase II (CAM-KII) and calcineurin, which activate nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and nuclear factor of activated T cells (NFAT), respectively. Solid black lines represent activation, while solid red lines represent inhibition. Double black lines represent indirect activation. Dashed lines indicate protein interactions when the WNT/β-catenin and mTOR signaling are not activated.