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dc.contributor.advisorYuluğ, Işık
dc.contributor.authorSunar, Gizem
dc.date.accessioned2021-02-15T06:32:46Z
dc.date.available2021-02-15T06:32:46Z
dc.date.copyright2021-02
dc.date.issued2021-02
dc.date.submitted2021-02-10
dc.identifier.urihttp://hdl.handle.net/11693/55127
dc.descriptionCataloged from PDF version of article.en_US
dc.descriptionThesis (M.S.): Bilkent University, Department of Molecular Biology and Genetics, İhsan Doğramacı Bilkent University, 2021.en_US
dc.descriptionIncludes bibliographical references (leaves 59-71).en_US
dc.description.abstractErbin is an ERBB2 interacting protein with roles in many signaling pathways. Breast cancer is one of the types of cancer that is affected by Erbin regulation. However, it is unclear how Erbin regulates the biological behavior and drug resistance of breast cancer cells. Some studies have claimed that Erbin promotes tumorigenesis and demonstrates oncogenic features in breast cancer, whereas others have indicated that it inhibits breast cancer development. The main aim of this study was to explore the role of the Erbin gene in breast cancer drug resistance. Bioinformatic analyses of breast cancer patient datasets have shown that a high level of Erbin expression predicts better survival in breast cancer patients treated with chemotherapy or targeted therapies while the Erbin level does not change the survival rates of untreated breast cancer patients. These analyses lead us to hypothesize that the Erbin expression level could alter the effect of the drug treatment and a reduced level of Erbin expression could promote resistance against doxorubicin and tamoxifen. In vitro studies have demonstrated that the protein expressions were apparently lower in MDA-MB-231 doxorubicin resistant (DoxR) and MCF-7 tamoxifen resistant (TamR) cells compared to non-resistant cell line counterparts. When the expression level of Erbin was downregulated by si-RNA transfection, it was observed that the protein level of the anti-apoptotic markers increased whereas apoptotic markers decreased in MDA-MB-231 cells. Proteins that promote cell survival and proliferation increased in Erbin downregulated MDA-MB-231 and MCF-7 cells. Besides, when Erbin was reduced, the viability of the MDA-MB-231 cells against doxorubicin increased but there was no significant change for tamoxifen in MCF-7 cells. Lastly, breast cancer patients with high Erbin expression that were treated with tamoxifen, chemotherapy or trastuzumab have higher levels of DNA damage, apoptosis and cell cycle arrest-related genes. On the contrary, patients with low Erbin expression have higher levels of cyclins, CDKs and anti-apoptotic genes. In conclusion, Erbin could play an important role in the drug resistance of breast cancer cells since the reduction in Erbin expression can promote drug resistance in these cells.en_US
dc.description.statementofresponsibilityby Gizem Sunaren_US
dc.format.extentxiv, 76 leaves : color charts, graphics ; 30 CM.en_US
dc.language.isoEnglishen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectERBINen_US
dc.subjectBreast canceren_US
dc.subjectDrug resistanceen_US
dc.subjectTamoxifenen_US
dc.subjectDoxorubicinen_US
dc.subjectApoptosisen_US
dc.titleFunctional analysis of Erbin gene in breast cancer drug resistanceen_US
dc.title.alternativeErbin geninin meme kanseri ilaç direncinde fonksiyonel analizien_US
dc.typeThesisen_US
dc.departmentDepartment of Molecular Biology and Geneticsen_US
dc.publisherBilkent Universityen_US
dc.description.degreeM.S.en_US
dc.identifier.itemidB150680


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