Suppression Of Bromodomaincontaining Protein 4 By Shrna: A New Approach For Cancer Treatment

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dc.contributor.authorKaya, Turan
dc.contributor.authorKahraman, Berke
dc.contributor.authorBazarov, Nurgeldi
dc.contributor.authorToker, Alperen S.
dc.contributor.authorCelik, Ayse
dc.contributor.authorCigdem, Sadik
dc.contributor.authorGündüz, Esra
dc.date.accessioned2025-10-24T18:06:43Z
dc.date.available2025-10-24T18:06:43Z
dc.date.issued2016
dc.departmentMalatya Turgut Özal Üniversitesi
dc.description.abstractPurpose: MYC is a transcription factor coding gene that is believed to control 15% of the genes in the entire human genome. The central role of c-MYC in cancer pathogenesis makes it a major therapeutic target in field of anticancer agent development. Methods: We targeted the acetyl-lysine binding modules or bromodomains, which are associated with c-MYC transcriptional activation. Results: Sequence specific inhibition of BET bromodomains with small hairpin RNAs (shRNAs) resulted in cessation of cellular proliferation in different cancer cell lines. Unlike previous studies on inhibition of bromodomains with selective small-molecule inhibitors, our study revealed the significant role of BET bromodomains in solid tumours and also highlighted the ease of RNA interference (RNAi) methodology for inhibition of bromodomain translation. Conclusion: The degree of influence of BET bromodomain inhibition on proliferation in five cancer cell lines established it as the major target in malignancies characterized by activation of c-MYC © 2021 Elsevier B.V., All rights reserved.
dc.identifier.doi10.25011/CIM.V39I6.27493
dc.identifier.endpage13
dc.identifier.issn0147-958X
dc.identifier.issn1488-2353
dc.identifier.issue6
dc.identifier.pmid27917784
dc.identifier.scopus2-s2.0-85047596661
dc.identifier.scopusqualityQ2
dc.identifier.startpage7
dc.identifier.urihttps://doi.rog/10.25011/CIM.V39I6.27493
dc.identifier.urihttps://hdl.handle.net/20.500.12899/3174
dc.identifier.volume39
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherThe Canadian Society for Clinical Investigation
dc.relation.ispartofClinical and Investigative Medicine
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzScopus_20251023
dc.subjectantineoplastic agent
dc.subjectBRD4 protein, human
dc.subjectlysine
dc.subjectMyc protein
dc.subjectMYC protein, human
dc.subjectnuclear protein
dc.subjectsmall interfering RNA
dc.subjecttranscription factor
dc.subjectchemistry
dc.subjectgene expression regulation
dc.subjectgene therapy
dc.subjectgenetics
dc.subjectHEK293 cell line
dc.subjectHeLa cell line
dc.subjectHep-G2 cell line
dc.subjectHT-29 cell line
dc.subjecthuman
dc.subjecthuman genome
dc.subjectMCF-7 cell line
dc.subjectmetabolism
dc.subjectmolecular cloning
dc.subjectneoplasm
dc.subjectplasmid
dc.subjectprocedures
dc.subjectprotein domain
dc.subjectRNA interference
dc.subjecttranscription initiation
dc.subjectAntineoplastic Agents
dc.subjectCloning, Molecular
dc.subjectGene Expression Regulation, Neoplastic
dc.subjectGenetic Therapy
dc.subjectGenome, Human
dc.subjectHEK293 Cells
dc.subjectHeLa Cells
dc.subjectHep G2 Cells
dc.subjectHT29 Cells
dc.subjectHumans
dc.subjectLysine
dc.subjectMCF-7 Cells
dc.subjectNeoplasms
dc.subjectNuclear Proteins
dc.subjectPlasmids
dc.subjectProtein Domains
dc.subjectProto-Oncogene Proteins c-myc
dc.subjectRNA Interference
dc.subjectRNA, Small Interfering
dc.subjectTranscription Factors
dc.subjectTranscriptional Activation
dc.titleSuppression Of Bromodomaincontaining Protein 4 By Shrna: A New Approach For Cancer Treatment
dc.typeArticle

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