Contribution of Autophagy to Epithelial Mesenchymal Transition Induction during Cancer Progression

dc.authoridCordani, Marco/0000-0001-9342-4862
dc.authoridAllameh, Abdolamir/0000-0003-0757-9572
dc.authoridKhosravi, Arezoo/0009-0006-6654-4133
dc.authoridZarrabi, Ali/0000-0003-0391-1769
dc.authoridStrippoli, Raffaele/0000-0003-3483-8381
dc.authorscopusid6506304690
dc.authorscopusid57202715531
dc.authorscopusid50861125300
dc.authorscopusid57202500098
dc.authorscopusid56405640000
dc.authorscopusid23483174100
dc.authorscopusid23483174100
dc.authorwosidCordani, Marco/ABF-4669-2021
dc.authorwosidAllameh, Abdolamir/E-3177-2010
dc.authorwosidKhosravi, Arezoo/JFK-3987-2023
dc.authorwosidZarrabi, Ali/U-2602-2019
dc.authorwosidStrippoli, Raffaele/J-2129-2018
dc.contributor.authorStrippoli, Raffaele
dc.contributor.authorNiayesh-Mehr, Reyhaneh
dc.contributor.authorAdelipour, Maryam
dc.contributor.authorKhosravi, Arezoo
dc.contributor.authorCordani, Marco
dc.contributor.authorZarrabi, Ali
dc.contributor.authorAllameh, Abdolamir
dc.contributor.otherGenetik ve Biyomühendislik / Genetic and Bio-Engineering
dc.date.accessioned2024-05-25T11:28:04Z
dc.date.available2024-05-25T11:28:04Z
dc.date.issued2024
dc.departmentOkan Universityen_US
dc.department-temp[Strippoli, Raffaele] Sapienza Univ Rome, Dept Mol Med, I-00161 Rome, Italy; [Strippoli, Raffaele] IRCCS, Natl Inst Infect Dis Lazzaro Spallanzani, I-00149 Rome, Italy; [Niayesh-Mehr, Reyhaneh; Allameh, Abdolamir] Tarbiat Modares Univ, Fac Med Sci, Dept Clin Biochem, POB 14115-331, Tehran, Iran; [Adelipour, Maryam] Ahvaz Jundishapur Univ Med Sci, Sch Med, Dept Clin Biochem, Ahvaz 6135715794, Iran; [Khosravi, Arezoo] Istanbul Okan Univ, Fac Engn & Nat Sci, Dept Genet & Bioengn, TR-34959 Istanbul, Turkiye; [Cordani, Marco] Univ Complutense Madrid, Fac Biol Sci, Dept Biochem & Mol Biol, Madrid 28040, Spain; [Cordani, Marco] Inst Invest Sanitarias San Carlos IdISSC, Madrid 28040, Spain; [Zarrabi, Ali] Istinye Univ, Fac Engn & Nat Sci, Dept Biomed Engn, TR-34396 Istanbul, Turkiye; [Zarrabi, Ali] Saveetha Univ, Saveetha Dent Coll & Hosp, Saveetha Inst Med & Tech Sci, Dept Res Analyt, Chennai 600077, Indiaen_US
dc.descriptionCordani, Marco/0000-0001-9342-4862; Allameh, Abdolamir/0000-0003-0757-9572; Khosravi, Arezoo/0009-0006-6654-4133; Zarrabi, Ali/0000-0003-0391-1769; Strippoli, Raffaele/0000-0003-3483-8381en_US
dc.description.abstractSimple Summary This manuscript focuses on the complex relationships between autophagy and epithelial mesenchymal transition (EMT) in cancer. Autophagy, a cellular degradation process, and EMT, a mechanism where epithelial cells acquire mesenchymal features, both play significant roles in cancer development. This review aims to explore how these processes interact, particularly how autophagy impacts cancer cell fate during EMT. The findings from this study are expected to contribute to a better understanding of cancer biology and could potentially impact cancer treatment strategies, as both autophagy and EMT are considered targets for therapy.Abstract 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.en_US
dc.description.sponsorshipThe Elite Research Committee of the NIMAD (National Institute for Medical Research Development)en_US
dc.description.sponsorshipNo Statement Availableen_US
dc.identifier.citation0
dc.identifier.doi10.3390/cancers16040807
dc.identifier.issn2072-6694
dc.identifier.issue4en_US
dc.identifier.pmid38398197
dc.identifier.scopus2-s2.0-85185907914
dc.identifier.scopusqualityQ2
dc.identifier.urihttps://doi.org/10.3390/cancers16040807
dc.identifier.urihttps://hdl.handle.net/20.500.14517/1128
dc.identifier.volume16en_US
dc.identifier.wosWOS:001168344700001
dc.identifier.wosqualityQ2
dc.institutionauthorKhosravi A.
dc.institutionauthorKhosravı, Arezoo
dc.language.isoen
dc.publisherMdpien_US
dc.relation.publicationcategoryDiğeren_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectautophagyen_US
dc.subjectepithelial mesenchymal transitionen_US
dc.subjectcell deathen_US
dc.subjectcell adhesion moleculesen_US
dc.subjectcell proliferationen_US
dc.subjectdifferentiationen_US
dc.titleContribution of Autophagy to Epithelial Mesenchymal Transition Induction during Cancer Progressionen_US
dc.typeReviewen_US
dspace.entity.typePublication
relation.isAuthorOfPublicationd1f338e7-edb6-47e4-bcd8-5ce91a9f40ba
relation.isAuthorOfPublication.latestForDiscoveryd1f338e7-edb6-47e4-bcd8-5ce91a9f40ba
relation.isOrgUnitOfPublication2b8689c6-2a28-45db-b81c-7f828c944e77
relation.isOrgUnitOfPublication.latestForDiscovery2b8689c6-2a28-45db-b81c-7f828c944e77

Files