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Fig. 9 | Molecular Cancer

Fig. 9

From: Crosstalk between autophagy and epithelial-mesenchymal transition and its application in cancer therapy

Fig. 9

Interplay between cytoskeleton and mitochondria. Cytoskeleton polymerization induced by EMT, which in turn supports mitochondrial fission that are essential for further sustain EMT process by providing energy supplies, and depolymerization of actin cytoskeleton is sufficient for reversing EMT phenotype. Massive activation of autophagy induces mitochondrial fusion and the reconstitution of mitochondrial network, which subsequently reduces the number of available free mitochondria and counteracts EMT. Mitochondrial protein BNIP3 potentially supported mitochondrial fission and turnover through stimulating mitophagy by directly binding to both mitochondria and the autophagosomal protein LC3, but also enhanced cytoskeleton polymerization. The interaction between BNIP3 and cadherin-6 (CDH6) drives EMT, restrains autophagy and promotes mitochondrial fission

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