Long noncoding RNA ERICD interacts with ARID3A via E2F1 and regulates migration and proliferation of osteosarcoma cells

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dc.authorscopusid56190917500
dc.authorscopusid55815636400
dc.authorscopusid23473166000
dc.authorscopusid56497061100
dc.authorscopusid35482179000
dc.authorscopusid6701544588
dc.authorscopusid56468900300
dc.contributor.authorArman, K.
dc.contributor.authorSaadat, Khandakar A.S.M.
dc.contributor.authorIğcı, Y.Z.
dc.contributor.authorBozgeyik, Esra
dc.contributor.authorİkeda, M.A.
dc.contributor.authorÇakmak, Ecir Ali
dc.contributor.authorArslan, A.
dc.date.accessioned2022-05-11T14:05:10Z
dc.date.available2022-05-11T14:05:10Z
dc.date.issued2020
dc.departmentFakülteler, Tıp Fakültesi, Dahili Tıp Bilimleri Bölümü, Tıbbi Genetik Ana Bilim Dalı
dc.description.abstractLong noncoding RNA (lncRNA) dysregulation is known to be taking part in majority of cancers, including osteosarcoma. In one of our previous studies, we showed that lncRNA MEG3 is being regulated by microRNA-664a (miR-664a) suppresses the migratory potential of osteosarcoma cells (U-2OS). We now report a novel lncRNA, namely, ERICD, which is linked to the transcription factor AT-rich interaction domain 3A (ARID3A) in U-2OS cells. We show that ARID3A binds to ERICD and indirectly interacts with each other via the E2F transcription factor 1 (E2F1). Furthermore, small interfering RNA (siRNA)-mediated knockdown of ERICD inhibited cell migration, formation of colonies, and proliferation in U-2OS cells. Overexpression of ARID3A inhibited cell migration, colony formation, and proliferation, whereas siRNA-mediated knockdown of ARID3A promoted cell migration, colony formation, and proliferation. Our findings indicate that ARID3A and lncRNA ERICD have plausible tumor suppressive and oncogenic functions, respectively, in osteosarcoma. Our data demonstrate the converse interaction between ARID3A and lncRNA ERICD that target DNA-binding proteins and dysregulation of their expression through E2F1 augments osteosarcoma progression. The cell rescue experiment also indicated E2F1 to be involved in the regulation of ARID3A and ERICD. © 2020 International Federation for Cell Biology
dc.description.sponsorship113S957; McGill University; Türkiye Bilimsel ve Teknolojik Araştirma Kurumu, TÜBITAK; Institut de Recherche Clinique De Montréal, IRCM
dc.description.sponsorshipKaifee Arman is a recipient of the Unger Hematology Research award and Jean Coutu Scholarship as Postdoc fellowship from McGill University and IRCM, respectively. We are highly grateful to Prof. Dr. Tarik Möröy (Director of the Hematopoiesis and Cancer research unit, IRCM) for his support and permission in performing several additional experiments using his lab resources. This research was supported by the grant from the Scientific and Technological Research Council of Turkey, TUBITAK (Grant number: 113S957).
dc.identifier.doi10.1002/cbin.11434
dc.identifier.endpage2274
dc.identifier.issn1065-6995
dc.identifier.issue11en_US
dc.identifier.pmid32749762
dc.identifier.scopus2-s2.0-85089259225
dc.identifier.scopusqualityQ1
dc.identifier.startpage2263
dc.identifier.urihttps://doi.org/10.1002/cbin.11434
dc.identifier.urihttps://hdl.handle.net/20.500.11776/4911
dc.identifier.volume44
dc.identifier.wosWOS:000557826000001
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorArslan, A.
dc.language.isoen
dc.publisherBlackwell Publishing Ltd
dc.relation.ispartofCell Biology International
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectARID3A
dc.subjectcolony formation
dc.subjectDNA-binding lncRNA
dc.subjectlncRNA ERICD
dc.subjectmigration
dc.subjectosteosarcoma
dc.subjectDNA binding protein
dc.subjectE2F transcription factor 1
dc.subjectlong noncoding RNA E2F1 regulated inhibitor of cell death
dc.subjectlong untranslated RNA
dc.subjecttranscription factor
dc.subjecttranscription factor AT rich interaction domain 3A
dc.subjecttranscription factor E2F
dc.subjectunclassified drug
dc.subjectARID3A protein, human
dc.subjectDNA binding protein
dc.subjectE2F1 protein, human
dc.subjectlong untranslated RNA
dc.subjecttranscription factor
dc.subjecttranscription factor E2F1
dc.subjectArticle
dc.subjectbinding site
dc.subjectcancer growth
dc.subjectcell migration
dc.subjectcell proliferation
dc.subjectcell viability
dc.subjectcolony formation
dc.subjectcontrolled study
dc.subjectdown regulation
dc.subjectgene expression regulation
dc.subjectgene function
dc.subjectgenetic correlation
dc.subjecthuman
dc.subjecthuman cell
dc.subjectosteosarcoma
dc.subjectpromoter region
dc.subjectprotein expression
dc.subjectprotein function
dc.subjectprotein RNA binding
dc.subjectregulatory mechanism
dc.subjectU2OS cell line
dc.subjectupregulation
dc.subjectapoptosis
dc.subjectbone tumor
dc.subjectcell motion
dc.subjectcell proliferation
dc.subjectgenetics
dc.subjectmetabolism
dc.subjectosteosarcoma
dc.subjectpathology
dc.subjecttumor cell line
dc.subjectApoptosis
dc.subjectBone Neoplasms
dc.subjectCell Line, Tumor
dc.subjectCell Movement
dc.subjectCell Proliferation
dc.subjectDNA-Binding Proteins
dc.subjectE2F1 Transcription Factor
dc.subjectGene Expression Regulation, Neoplastic
dc.subjectHumans
dc.subjectOsteosarcoma
dc.subjectRNA, Long Noncoding
dc.subjectTranscription Factors
dc.titleLong noncoding RNA ERICD interacts with ARID3A via E2F1 and regulates migration and proliferation of osteosarcoma cells
dc.typeArticle

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