AKT-mediated phosphorylation of TWIST1 is essential for breast cancer cell metastasis

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dc.contributor.authorErtosun, Mustafa Gokhan
dc.contributor.authorPehlivanoglu, Suray
dc.contributor.authorDilmac, Sayra
dc.contributor.authorTanriover, Gamze
dc.contributor.authorOzes, Osman Nidai
dc.date.accessioned2024-02-23T14:35:28Z
dc.date.available2024-02-23T14:35:28Z
dc.date.issued2020
dc.departmentNEÜen_US
dc.description.abstractPreviously, it was shown that human TWIST1 (basic helix-loop-helix (b-HLH) is phosphorylated by Akt kinase at S42, T121, and S123. To show in vivo effect of these phosphorylations, we created mouse TWIST1 expression vector and converted the codons of S42, T125, and S127 to unphosphorylatable alanine and phosphorylation mimicking Glutamic acid. We hypothesized that alanine mutants would inhibit the metastatic ability of 4T1 cells while glutamic acid mutants would convert nonmetastatic 67NR cells into metastatic phenotype. To confirm this hypothesis, we created metastatic 4T1 and nonmetastatic 67NR cells expressing alanine mutants and glutamic acid mutants mouse TWIST1, respectively. Then, we injected 1 x 10(6) 67NR and 1 x 10(5) 4T1 cells overexpressing mutants of TWIST1 into the breast tissue of BALB/c mice. At the end of the 4th week, we sacrificed the animals, determined the numbers of tumors at lungs and liver. Although 67NR cells overexpressing wild-type TWIST1 did not show any metastasis, cells overexpressing S42E and T125E mutants showed 15-30 macroscopic metastasis to liver and lungs. Parallel to this, 4T1 cells expressing S42A and T125A mutants of TWIST1 showed no macroscopic metastasis. Our results indicate that phosphorylation of S42 and T125 by AKT is essential for TWIST1-mediated tumor growth and metastasis.en_US
dc.identifier.doi10.3906/biy-1912-74
dc.identifier.endpage+en_US
dc.identifier.issn1300-0152
dc.identifier.issn1303-6092
dc.identifier.issue4en_US
dc.identifier.pmid32922123en_US
dc.identifier.scopus2-s2.0-85089669270en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage158en_US
dc.identifier.urihttps://doi.org/10.3906/biy-1912-74
dc.identifier.urihttps://hdl.handle.net/20.500.12452/16038
dc.identifier.volume44en_US
dc.identifier.wosWOS:000582626100004en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherTubitak Scientific & Technological Research Council Turkeyen_US
dc.relation.ispartofTurkish Journal Of Biologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectTwist1en_US
dc.subjectBreast Canceren_US
dc.subjectMetastasisen_US
dc.titleAKT-mediated phosphorylation of TWIST1 is essential for breast cancer cell metastasisen_US
dc.typeArticleen_US

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