Contribution of Autophagy to Epithelial Mesenchymal Transition Induction during Cancer Progression

  1. Strippoli, Raffaele 67
  2. Niayesh-Mehr, Reyhaneh 1
  3. Adelipour, Maryam 2
  4. Khosravi, Arezoo 3
  5. Cordani, Marco 45
  6. Zarrabi, Ali 89
  7. Allameh, Abdolamir 1
  1. 1 Department of Clinical Biochemistry, Faculty of Medical Science, Tarbiat Modares University, Tehran P.O. Box 14115-331, Iran
  2. 2 Department of Clinical Biochemistry, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz 61357-15794, Iran
  3. 3 Department of Genetics and Bioengineering, Faculty of Engineering and Natural Sciences, Istanbul Okan University, Istanbul 34959, Türkiye
  4. 4 Department of Biochemistry and Molecular Biology, Faculty of Biological Sciences, Complutense University of Madrid, 28040 Madrid, Spain
  5. 5 Instituto de Investigaciones Sanitarias San Carlos (IdISSC), 28040 Madrid, Spain
  6. 6 Department of Molecular Medicine, Sapienza University of Rome, 00161 Rome, Italy
  7. 7 National Institute for Infectious Diseases “Lazzaro Spallanzani”, I.R.C.C.S., 00149 Rome, Italy
  8. 8 Department of Biomedical Engineering, Faculty of Engineering and Natural Sciences, Istinye University, Istanbul 34396, Türkiye
  9. 9 Department of Research Analytics, Saveetha Dental College and Hospitals, Saveetha Institute of Medical and Technical Sciences, Saveetha University, Chennai 600077, India
Revista:
Cancers

ISSN: 2072-6694

Año de publicación: 2024

Volumen: 16

Número: 4

Páginas: 807

Tipo: Artículo

DOI: 10.3390/CANCERS16040807 GOOGLE SCHOLAR lock_openAcceso abierto editor

Otras publicaciones en: Cancers

Resumen

Epithelial Mesenchymal Transition (EMT) is a dedifferentiation process implicated in many physio-pathological conditions including tumor transformation. EMT is regulated by several extracellular mediators and under certain conditions it can be reversible. Autophagy is a conserved catabolic process in which intracellular components such as protein/DNA aggregates and abnormal organelles are degraded in specific lysosomes. In cancer, autophagy plays a controversial role, acting in different conditions as both a tumor suppressor and a tumor-promoting mechanism. Experimental evidence shows that deep interrelations exist between EMT and autophagy-related pathways. Although this interplay has already been analyzed in previous studies, understanding mechanisms and the translational implications of autophagy/EMT need further study. The role of autophagy in EMT is not limited to morphological changes, but activation of autophagy could be important to DNA repair/damage system, cell adhesion molecules, and cell proliferation and differentiation processes. Based on this, both autophagy and EMT and related pathways are now considered as targets for cancer therapy. In this review article, the contribution of autophagy to EMT and progression of cancer is discussed. This article also describes the multiple connections between EMT and autophagy and their implication in cancer treatment.

Información de financiación

Financiadores

  • The Elite Research Committee of the NIMAD
    • 4002451
  • Spanish Ministry of Science and Innovation, Agencia Estatal de Investigación
    • RYC2021–031003-I
  • Italian ministry of University

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