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dc.contributor.advisorGary Stein
dc.contributor.authorHong, Deli
dc.date2022-08-11T08:08:46.000
dc.date.accessioned2022-08-23T16:07:52Z
dc.date.available2022-08-23T16:07:52Z
dc.date.issued2017-12-12
dc.date.submitted2018-01-24
dc.identifier.doi10.13028/M21Q2F
dc.identifier.urihttp://hdl.handle.net/20.500.14038/32333
dc.description.abstractBreast cancer remains the most common malignant disease in women worldwide. Despite the advantages of early detection and improved treatments, studies into the mechanisms that initiate and drive breast cancer progression are still required. Recent studies have identified RUNX1, which is an essential transcription factor for hematopoiesis, is one of the most frequently mutated genes in breast cancer patients. However, the role of RUNX1 in the mammary gland is understudied. In this dissertation, we examined the role of RUNX1 in both normal mammary epithelial and breast cancer cells. Our in vitro studies demonstrated that RUNX1 inhibits epithelial to mesenchymal transition (EMT), migration, and invasion, reflecting its tumor suppressor activity, which was confirmed in vivo. Moreover, RUNX1 also contributes significantly to inhibition of the phenotypes of breast cancer stem cells (CSC), which is responsible for metastasis and tumor relapse. We showed that Runx1 overexpression reduces the tumorsphere formation and cancer stem cell population. Overall, our studies provide mechanistic evidence for RUNX1 repression of EMT in mammary cells, anti-tumor activity in vivo and regulation of CSC-like properties in breast cancer. Our results highlight crucial roles for RUNX1 in preventing epithelial to mesenchymal transition and tumor progression in breast cancer. This RUNX1 mediated mechanism points to novel intervention strategies for early stage breast cancer.
dc.language.isoen_US
dc.rightsCopyright is held by the author, with all rights reserved.
dc.subjectRunx1
dc.subjectBreast Cancer
dc.subjectEpithelial to Mesenchymal Transition (EMT)
dc.subjectCancer Stem Cell
dc.subjectCancer Biology
dc.subjectCell Biology
dc.titleRUNX1 Control of Mammary Epithelial and Breast Cancer Cell Phenotypes
dc.typeDoctoral Dissertation
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1955&context=gsbs_diss&unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_diss/949
dc.legacy.embargo2019-01-24T00:00:00-08:00
dc.identifier.contextkey11415069
refterms.dateFOA2022-08-24T04:17:29Z
html.description.abstract<p>Breast cancer remains the most common malignant disease in women worldwide. Despite the advantages of early detection and improved treatments, studies into the mechanisms that initiate and drive breast cancer progression are still required. Recent studies have identified RUNX1, which is an essential transcription factor for hematopoiesis, is one of the most frequently mutated genes in breast cancer patients. However, the role of RUNX1 in the mammary gland is understudied.</p> <p>In this dissertation, we examined the role of RUNX1 in both normal mammary epithelial and breast cancer cells. Our <em>in vitro</em> studies demonstrated that RUNX1 inhibits epithelial to mesenchymal transition (EMT), migration, and invasion, reflecting its tumor suppressor activity, which was confirmed <em>in vivo</em>. Moreover, RUNX1 also contributes significantly to inhibition of the phenotypes of breast cancer stem cells (CSC), which is responsible for metastasis and tumor relapse. We showed that Runx1 overexpression reduces the tumorsphere formation and cancer stem cell population. Overall, our studies provide mechanistic evidence for RUNX1 repression of EMT in mammary cells, anti-tumor activity <em>in vivo</em> and regulation of CSC-like properties in breast cancer.</p> <p>Our results highlight crucial roles for RUNX1 in preventing epithelial to mesenchymal transition and tumor progression in breast cancer. This RUNX1 mediated mechanism points to novel intervention strategies for early stage breast cancer.</p>
dc.identifier.submissionpathgsbs_diss/949
dc.contributor.departmentCell Biology
dc.description.thesisprogramCell Biology
dc.identifier.orcid0000-0001-9863-4877


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