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dc.contributor.advisorZeyen Øyås, Lisa
dc.contributor.advisorMikkola, Ingvild
dc.contributor.authorBrown, Rosaline
dc.date.accessioned2022-06-01T05:33:47Z
dc.date.available2022-06-01T05:33:47Z
dc.date.issued2022-05-12en
dc.description.abstractWhile targeted therapy exists for ER-positive breast cancers, the treatment option for TNBC is conventional chemotherapy giving a poorer prognosis. It is therefore of interest to study molecular mechanisms and differences between MCF7 (ER-positive) and MDA-MB-231 (ER, PR, and HER2- negative). These cell lines are in vitro representative models for luminal A (non-aggressive) and basal-like (aggressive) breast tumors. In this study, the cell lines are stimulated with Anisomycin and Dexamethasone, and their response is observed and compared in relation to the P38 MAPK signaling pathway and GR. To achieve molecular and functional analysis of the cell lines Western Blot, proliferation assays, cell viability assays and a scratch wound assay was achieved to compare the cell lines, respectively. Anisomycin is a rapid and potent activator of p38 MAPK and inhibits proliferation in both cell lines, but the activation of the p38 MAPK signalling pathway is different as shown by the phosphorylation kinetics of the downstream targets GR (S134) and HSP27. Results also show that Dex stimulation and activation of GR in the MDA-MB-231 cells cause increased proliferation, but for MCF7 the effect of Dex with regard to proliferation was minor. Further, migration seemed to be positively affected by Dex in MCF7 and negatively affected by Dex in MDA-MB-231 cells. These findings indicate that activation of the p38 MAPK pathway in MCF7 and MDA-MB-231 cells will cause different downstream responses, among them the kinetics of the phosphorylation of GR. It will be interesting to see if these differences could be further investigated with the intention to develop targeted therapy for TNBC cells.en_US
dc.identifier.urihttps://hdl.handle.net/10037/25329
dc.language.isoengen_US
dc.publisherUiT Norges arktiske universitetno
dc.publisherUiT The Arctic University of Norwayen
dc.rights.holderCopyright 2022 The Author(s)
dc.rights.urihttps://creativecommons.org/licenses/by-nc-sa/4.0en_US
dc.rightsAttribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)en_US
dc.subject.courseIDFAR-3911
dc.subjectp38MAPKen_US
dc.subjectGRen_US
dc.subjectBreast Canceren_US
dc.subjectDexamethasoneen_US
dc.subjectAnisomycinen_US
dc.subjectCell signalingen_US
dc.titleFunctional analysis of signaling pathways activated by Anisomycin and Dexamethasone in two different breast cancer cell linesen_US
dc.typeMastergradsoppgaveno
dc.typeMaster thesisen


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Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)