EMT and Inflammation: Crossroads in HCC

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dc.authoridAlotaibi, Hani/0000-0001-7423-9653
dc.authoridSengez, Burcu/0000-0002-1833-4135
dc.authoridCarr, Brian/0000-0002-6111-5077
dc.authorwosidAlotaibi, Hani/R-3158-2016
dc.contributor.authorSengez, Burcu
dc.contributor.authorCarr, Brian, I
dc.contributor.authorAlotaibi, Hani
dc.date.accessioned2024-08-04T20:51:35Z
dc.date.available2024-08-04T20:51:35Z
dc.date.issued2023
dc.departmentİnönü Üniversitesien_US
dc.description.abstractHepatocellular carcinoma is one of the major causes of cancer-related deaths worldwide and is associated with several inflammatory mediators, since 90% of HCCs occur based on chronic hepatitis B or C, alcoholism or increasingly metabolic syndrome-associated inflammation. EMT is a physiological process, with coordinated changes in epithelial gene signatures and is regulated by multiple factors, including cytokines and growth factors such as TGF beta, EGF, and FGF. Recent reports propose a strong association between EMT and inflammation, which is also correlated with tumor aggressiveness and poor outcomes. Cellular heterogeneity results collectively as an outcome of EMT, inflammation, and the tumor microenvironment, and it plays a fundamental role in the progression, complexity of cancer, and chemoresistance. In this review, we highlight recent developments concerning the association of EMT and inflammation in the context of HCC progression. Identifying potential EMT-related biomarkers and understanding EMT regulatory molecules will likely contribute to promising developments in clinical practice and will be a valuable tool for predicting metastasis in general and specifically in HCC.en_US
dc.description.sponsorshipNIH [CA 82723]; TUBITAK [114Z245, 117Z223, 120N556, 219Z034]en_US
dc.description.sponsorshipThis work was supported in part by NIH grant number CA 82723 (to BIC) and TUBITAK grant numbers 114Z245, 117Z223, 120N556, and 219Z034 (to H.A).en_US
dc.identifier.doi10.1007/s12029-021-00801-z
dc.identifier.endpage212en_US
dc.identifier.issn1941-6628
dc.identifier.issn1941-6636
dc.identifier.issue1en_US
dc.identifier.pmid35020133en_US
dc.identifier.scopus2-s2.0-85122828298en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage204en_US
dc.identifier.urihttps://doi.org/10.1007/s12029-021-00801-z
dc.identifier.urihttps://hdl.handle.net/11616/100413
dc.identifier.volume54en_US
dc.identifier.wosWOS:000741862300001en_US
dc.identifier.wosqualityN/Aen_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSpringeren_US
dc.relation.ispartofJournal of Gastrointestinal Canceren_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectEMTen_US
dc.subjectInflammationen_US
dc.subjectHCCen_US
dc.subjectLiver canceren_US
dc.titleEMT and Inflammation: Crossroads in HCCen_US
dc.typeReview Articleen_US

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