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Fig. 6 | Molecular Cancer

Fig. 6

From: Crosstalk between autophagy inhibitors and endosome-related secretory pathways: a challenge for autophagy-based treatment of solid cancers

Fig. 6

Multivesicular bodies and autophagy. After maturation of early endosomes to multivesicular bodies (MVBs), MVBs can fuse with the plasma membrane to release intraluminal vesicles (ILVs) to the extracellular space as exosomes. With the help of specific proteins, MVBs are trafficked towards the plasma membrane and/or lysosome. Under certain conditions, MVBs can fuse with autophagosomes to generate hybrid organelles called amphisomes. Amphisomes contain typical autophagosomal markers such as lipidated LC3, and due to their origin from endosomes, they also contain endosomal markers such as CD63, RAB5, RAB7, and RAB11. The fusion of MVBs with the lysosome (direct or via autophagosome) results in autophagic degradation. The MVBs-related secretion and autophagy pathways are connected via many proteins, including RAB GTPases, ESCRTs, SNAREs, Beclin1, ATG proteins, and LC3

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