ABSTRACT
Autophagy is a self-renewing cellular process by which defective proteins and aged organs are eliminated. It is noteworthy that autophagy correlates with the initiation and progression of cancer. During epithelial-mesenchymal transition (EMT), cells with epithelial phenotype gain mesenchymal characteristics, thus facilitate invasion and metastasis. Autophagy may suppress EMT by the following mechanisms, such as decreasing hypoxia inducible factor-1 (HIF-1) in hypoxia to downregulate transcription of EMT related genes, regulating TGF-β/Smad signaling pathway negatively, utilizing selective autophagy adaptor, p62, to modulate EMT transcription factors. Further studies of the association between autophagy and EMT may contribute to indentify new targets of cancer therapy.
ABSTRACT
Autophagy is a self-renewing cellular process by which defective proteins and aged organs are eliminated. It is noteworthy that autophagy correlates with the initiation and progression of cancer. During epithelial-mesenchymal transition (EMT), cells with epithelial phenotype gain mesenchymal characteristics, thus facilitate invasion and metastasis. Autophagy may suppress EMT by the following mechanisms, such as decreasing hypoxia inducible factor-1 (HIF-1) in hypoxia to downregulate transcription of EMT related genes, regulating TGF-β/Smad signaling pathway negatively, utilizing selective autophagy adaptor, p62, to modulate EMT transcription factors. Further studies of the association between autophagy and EMT may contribute to indentify new targets of cancer therapy.