Autophagy and mTOR pathways in mouse embryonic stem cell, lung cancer and somatic fibroblast cell lines

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dc.contributor.authorOltulu, Fatih
dc.contributor.authorKocaturk, Duygu C.
dc.contributor.authorAdali, Yasemin
dc.contributor.authorOzdil, Berrin
dc.contributor.authorAcikgoz, Eda
dc.contributor.authorGurel, Cevik
dc.contributor.authorYavasoglu, N. Ulku Karabay
dc.contributor.authorAktug, Huseyin
dc.date.accessioned2019-10-27T09:41:06Z
dc.date.available2019-10-27T09:41:06Z
dc.date.issued2019
dc.departmentEge Üniversitesien_US
dc.description.abstractEmbryonic developmental stages and regulations have always been one of the most intriguing aspects of science. Since the cancer stem cell discovery, striking for cancer development and recurrence, embryonic stem cells and control mechanisms, as well as cancer cells and cancer stem cell control mechanisms become important research materials. It is necessary to reveal the similarities and differences between somatic and cancer cells which are formed of embryonic stem cells divisions and determinations. For this purpose, mouse embryonic stem cells (mESCs), mouse skin fibroblast cells (MSFs) and mouse lung squamous cancer cells (SqLCCs) were grown in vitro and the differences between these three cell lines signalling regulations of mechanistic target of rapamycin (mTOR) and autophagic pathways were demonstrated by immunofluorescence and real-time polymerase chain reaction. Expressional differences were clearly shown between embryonic, cancer and somatic cells that mESCs displayed higher expressional level of Atg10, Hdac1 and Cln3 which are related with autophagic regulation and Hsp4, Prkca, Rhoa and ribosomal S6 genes related with mTOR activity. LC3 and mTOR protein levels were lower in mESCs than MSFs. Thus, the mechanisms of embryonic stem cell regulation results in the formation of somatic tissues whereas that these cells may be the causative agents of cancer in any deterioration.en_US
dc.description.sponsorshipEge UniversitesiEge University [16-TIP-045]; Ege University Scientific Research Projects coordination unitEge University [16-TIP-045]en_US
dc.identifier.doi10.1002/jcb.29110en_US
dc.identifier.endpage18076en_US
dc.identifier.issn0730-2312
dc.identifier.issn1097-4644
dc.identifier.issue10en_US
dc.identifier.pmid31148273en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage18066en_US
dc.identifier.urihttps://doi.org/10.1002/jcb.29110
dc.identifier.urihttps://hdl.handle.net/11454/28579
dc.identifier.volume120en_US
dc.identifier.wosWOS:000483551100158en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherWileyen_US
dc.relation.ispartofJournal of Cellular Biochemistryen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectautophagyen_US
dc.subjectcancer cellsen_US
dc.subjectembryonic stem cellen_US
dc.subjectmTORen_US
dc.subjectsomatic cellen_US
dc.titleAutophagy and mTOR pathways in mouse embryonic stem cell, lung cancer and somatic fibroblast cell linesen_US
dc.typeArticleen_US

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