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Upregulation of dual-specificity phosphatase-26 is required for transforming growth factor β1(TGFβ1)-induced Epithelial-mesenchymal transition in A549 and PANC1 cells

dc.contributor.authorGüler, Sabire
dc.contributor.authorZık, Berrin
dc.contributor.authorYalçın, Abdullah
dc.contributor.buuauthorGÜLER, SABİRE
dc.contributor.buuauthorZIK, BERRİN
dc.contributor.buuauthorYALÇIN, ABDULLAH
dc.contributor.departmentVeteriner Fakültesi
dc.contributor.departmentBiyokimya Ana Bilim Dalı
dc.contributor.orcid0000-0002-7367-6859
dc.contributor.orcid0000-0001-8519-8375
dc.contributor.researcheridAAH-9810-2021
dc.contributor.researcheridABI-4164-2020
dc.contributor.researcheridAAH-8807-2021
dc.contributor.researcheridA-5261-2016
dc.date.accessioned2024-10-24T09:12:06Z
dc.date.available2024-10-24T09:12:06Z
dc.date.issued2022-09-02
dc.description.abstractBackground Transforming Growth Factor beta (TGF beta) proteins are potent inducers of the epithelial-mesenchymal transition (EMT) in tumor cells. Although mitogen-activated protein kinase (MAPK) family has been shown to be involved in TGF beta-induced EMT, role of Dual Specificity Phosphatases (DUSP), key regulators of MAPK activity, in TGF beta-induced EMT is largely unkonwn.Methods and results Real-time qPCR analyses were performed to determine the effect of TGF beta 1 on expression of EMT genes and DUSP proteins in the non-small cell lung cancer model A549 and pancreatic adenocarcinoma model PANC1 cells. Western blot analyses were conducted to study the changes in protein levels of EMT proteins and select DUSP proteins, as well as phosphorylations of MAPK proteins upon TGF beta 1 stimulation. Small interfering RNA (siRNA) was utilized to reduce expressions of DUSP genes. We observed that the EMT phenotype coincided with increases in phosphorylations of the MAPK proteins ERK1/2, p38MAPK, and JNK upon TGF beta 1 stimulation. Real-time qPCR analysis showed increases in DUSP15 and DUSP26 mRNA levels and Western blot analysis confirmed the increase in DUSP26 protein levels in both A549 and PANC1 cells treated with TGF beta 1 relative to control. Silencing of DUSP26 expression by siRNA markedly suppressed the effect of TGF beta 1 on E-cadherin and mesenchymal genes in the cells.Conclusions Data provided suggest that TGF beta 1 modulates the expression of DUSP genes and that upregulation of DUSP26 may be required for TGF beta 1-promoted EMT in A549 and PANC1 cells. Further studies should be carried out to elucidate the requirement of individual DUSPs in TGF beta 1-associated EMT in tumor cells.
dc.identifier.doi10.1007/s11033-022-07893-1
dc.identifier.endpage10204
dc.identifier.issn0301-4851
dc.identifier.issue11
dc.identifier.startpage10195
dc.identifier.urihttps://doi.org/10.1007/s11033-022-07893-1
dc.identifier.urihttps://link.springer.com/article/10.1007/s11033-022-07893-1
dc.identifier.urihttps://hdl.handle.net/11452/47005
dc.identifier.volume49
dc.identifier.wos000849163800002
dc.indexed.wosWOS.SCI
dc.language.isoen
dc.publisherSpringer
dc.relation.journalMolecular Biology Reports
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi
dc.relation.tubitak118Z092
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectGene-expression
dc.subjectCancer
dc.subjectMapk
dc.subjectSmad
dc.subjectOverexpression
dc.subjectResistance
dc.subjectInduction
dc.subjectEmt
dc.subjectTgf beta 1
dc.subjectEpithelial-mesenchymal transition
dc.subjectDual-specifity phosphatases
dc.subjectMapk
dc.subjectDusp26
dc.subjectBiochemistry & molecular biology
dc.titleUpregulation of dual-specificity phosphatase-26 is required for transforming growth factor β1(TGFβ1)-induced Epithelial-mesenchymal transition in A549 and PANC1 cells
dc.typeArticle
dspace.entity.typePublication
local.contributor.departmentVeteriner Fakültesi/Histoloji ve Embriyoloji Ana Bilim Dalı
local.contributor.departmentVeteriner Fakültesi/Biyokimya Ana Bilim Dalı
relation.isAuthorOfPublication65c482b5-8e65-438b-934f-90fef538a967
relation.isAuthorOfPublicationa30427a9-dc3b-4196-927b-d5b5b4e35e1f
relation.isAuthorOfPublication24332407-6513-4c39-92c2-21a376f853b1
relation.isAuthorOfPublication.latestForDiscovery65c482b5-8e65-438b-934f-90fef538a967

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