Modulation of YAP1 expression and other related signaling pathways in HepG2 cells by extracellular matrix, contact inhibition and cell density

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dc.authorid0000-0002-4474-7371en_US
dc.authorid0000-0002-7526-8496en_US
dc.authorid0000-0002-4605-1167en_US
dc.authorid0000-0002-4605-1167en_US
dc.authorid0000-0001-5114-8660en_US
dc.contributor.authorAktas, Ranan
dc.contributor.authorAkbulut, Zeynep
dc.contributor.authorMaraş, Hatice
dc.contributor.authorÇakıl Dönmez, Yaprak
dc.contributor.authorKayalı, Damla
dc.contributor.authorKaragoz Koroglu, Ayca
dc.contributor.authorSitar, Mustafa Erinc
dc.contributor.authorKısakol, Batuhan
dc.contributor.authorBaysan, Mehmet
dc.date.accessioned2024-07-12T21:13:56Z
dc.date.available2024-07-12T21:13:56Z
dc.date.issued2022en_US
dc.departmentFakülteler, Tıp Fakültesien_US
dc.description.abstractBackground: Hippo-YAP pathway is a key modulator in liver development, regeneration and the metabolism . Cell density, cell contact, the actin cytoskeleton, and extracellular matrix (ECM) composition have been shown to be involved in regulation of this pathway . The intervention of this pathway in hepatocellular carcinoma remains a central focus . The study aimed to examine how YAP1 integrate mechanical cues with the response to signal transduction pathways and to multiple aspects of cell behavior, proliferation, protein/lipid secretion, apoptosis/necrosis, adhesion, and stemness . Methods: HepG2 cells were cultured on uncoated (1), or Type I collagen (2), standard matrigel (3) or high concentration-matrigel coated surfaces (4) for 6 weeks . The cells were examined at 60% or 100%confluency, and at the end of each week by qRT-PCR, confocal microscopy, MTT, ELISA, and flow cytometry. Expression of 84 genes including YAP1, cell adhesion molecules (Inhibin, Cadherin, Na-K ATPase), apoptotic/necrotic changes, viability, protein/ lipid secretion, and existence of 7 different cancer stem cells were compared with Spearmen correlation test . Results: YAP1 gene expression changed significantly in Group1. Contact inhibition with 100% confluency caused deacrease at YAP1 in all groups . It was always low in group4 when compared with the others . Strong correlation between the YAP1, Actin-beta, and most of the genes in TGFB, AKT-P13 and RAS/RAF/MAPK pathways were clear (Graph I) . Positive correlation between cholesterol /LDL/HDL secretion; negative correlation between protein secretion, necrosis and CD133 (+) cells were notable . Conclusion: Herein, we described for the first time how liver cancer cells translate complex and dynamic changes at the external cues into signaling conduits that impact on YAP and other related gene expressions as well as on metabolic and morphological features of the cells . The study demonstrated the striking changes through the receptor of integrin alpha2beta1 that is stimulated by type I collagen . Changes in group 3 and 4 suggest that growth factors in stroma is another important factor at the response related to YAP1 expression. To our knowledge, this is the first study demonstrates Actin and YAP1 interaction at the gene expression level .en_US
dc.identifier.citationAktaş, R., Akbulut, Z., vd. (2022). Modulation of YAP1 expression and other related signaling pathways in HepG2 cells by extracellular matrix, contact inhibition and cell density. AASLD The Liver Meeting içinde (ss.239A).en_US
dc.identifier.startpage239Aen_US
dc.identifier.urihttps://aasld.confex.com/aasld/2020/meetingapp.cgi/Paper/23145
dc.identifier.urihttps://hdl.handle.net/20.500.12415/4576
dc.institutionauthorAktaş, Ranan
dc.institutionauthorAkbulut, Zeynep
dc.institutionauthorÇakıl Dönmez, Yaprak
dc.institutionauthorKayalı, Damla
dc.institutionauthorSitar, Mustafa Erinç
dc.language.isoenen_US
dc.publisherAmerican Association for the Study of Liver Diseasesen_US
dc.relation.ispartofAASLD The Liver Meetingen_US
dc.relation.publicationcategoryUluslararası Konferans Öğesien_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.snmzKY07215
dc.titleModulation of YAP1 expression and other related signaling pathways in HepG2 cells by extracellular matrix, contact inhibition and cell densityen_US
dc.typeConference Object
dspace.entity.typePublication

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