{"id":{"repo_id":"ohiolink","oai_identifier":"oai:etd.ohiolink.edu:ohiou1366239912"},"canonical_url":"https://search.dev.ndltd.org/etd/ohiolink/oai:etd.ohiolink.edu:ohiou1366239912","repository":{"repo_id":"ohiolink","name":"OhioLINK","base_url":"https://etd.ohiolink.edu/acprod/odb_etd/ws/oai/oai"},"display":{"title":"Breast Cancer Cells Acquire a Stem-Like Phenotype by TGFß1/EGF Induced Epithelial-Mesenchymal Transition","abstract":"Epithelial-Mesenchymal Transition (EMT) is a key developmental program that is often activated during cancer invasion and metastasis. In breast cancer, EMT is associated with cancer stem cell properties including expression of the stem cell antigenic profile, over-expression of transcription factors involved in EMT, adhesion to bone marrow endothelium and increased migratory capabilities. Research suggests that transforming growth factor (TGF)-ß and Epidermal Growth Factor (EGF) induces EMT and allows cancer cells to become more stem-like. We have shown that TGF-ß1 alone can partly increase expression of EMT-related transcription factors in BT-20 and MCF-7 cells. Furthermore, EGF alone can induce a stem cell-like phenotype in BT-20 cells and promote adhesion on human umbilical vein endothelial cells (HUVECs) but cannot promote expression of EMT-related transcription factors in BT-20 cells. A combination of EGF and TGF-ß1 can promote expression of EMT-related transcription factors in BT-20 cells. These results indicate that a combination of EGF and TGF-ß1 can induce EMT and cause acquisition of a stem-like phenotype by human breast cancer cell lines.","abstract_html":"Epithelial-Mesenchymal Transition (EMT) is a key developmental program that is often activated during cancer invasion and metastasis. In breast cancer, EMT is associated with cancer stem cell properties including expression of the stem cell antigenic profile, over-expression of transcription factors involved in EMT, adhesion to bone marrow endothelium and increased migratory capabilities. Research suggests that transforming growth factor (TGF)-ß and Epidermal Growth Factor (EGF) induces EMT and allows cancer cells to become more stem-like. We have shown that TGF-ß1 alone can partly increase expression of EMT-related transcription factors in BT-20 and MCF-7 cells. Furthermore, EGF alone can induce a stem cell-like phenotype in BT-20 cells and promote adhesion on human umbilical vein endothelial cells (HUVECs) but cannot promote expression of EMT-related transcription factors in BT-20 cells. A combination of EGF and TGF-ß1 can promote expression of EMT-related transcription factors in BT-20 cells. These results indicate that a combination of EGF and TGF-ß1 can induce EMT and cause acquisition of a stem-like phenotype by human breast cancer cell lines.","abstract_has_math":false,"creators":["Xiong, Chengkai"],"institution":"Ohio University","degree_name":"Master of Science (MS)","degree_level":"masters","degree_discipline":"Biomedical Engineering (Engineering and Technology)","degree_department":null,"school":null,"contributors":["Benencia, Fabian"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2013,"date_issued":"2013-06-17","date_published":"2013-06-17","updated_at":"2026-07-24T03:37:46Z","subjects":["Biomedical Engineering","Epithelial-Mesenchymal Transition","stem cell","transforming growth factor","Epidermal Growth Factor","breast cancer"],"languages":["English"],"rights":["unrestricted","This thesis or dissertation is protected by copyright: all rights reserved. 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We have shown that TGF-ß1 alone can partly increase expression of EMT-related transcription factors in BT-20 and MCF-7 cells. Furthermore, EGF alone can induce a stem cell-like phenotype in BT-20 cells and promote adhesion on human umbilical vein endothelial cells (HUVECs) but cannot promote expression of EMT-related transcription factors in BT-20 cells. A combination of EGF and TGF-ß1 can promote expression of EMT-related transcription factors in BT-20 cells. These results indicate that a combination of EGF and TGF-ß1 can induce EMT and cause acquisition of a stem-like phenotype by human breast cancer cell lines."]},{"key":"dc:format","label":"Dc Format","values":["application/pdf","p.55","1.93 MB"]},{"key":"dc:title","label":"Title","values":["Breast Cancer Cells Acquire a Stem-Like Phenotype by TGFß1/EGF Induced Epithelial-Mesenchymal Transition"]}]}],"canonical_facts":{"dc:contributor":["Benencia, Fabian"],"dc:creator":["Xiong, Chengkai"],"dc:date":["2013-06-17"],"dc:description":["Epithelial-Mesenchymal Transition (EMT) is a key developmental program that is often activated during cancer invasion and metastasis. In breast cancer, EMT is associated with cancer stem cell properties including expression of the stem cell antigenic profile, over-expression of transcription factors involved in EMT, adhesion to bone marrow endothelium and increased migratory capabilities. Research suggests that transforming growth factor (TGF)-ß and Epidermal Growth Factor (EGF) induces EMT and allows cancer cells to become more stem-like. We have shown that TGF-ß1 alone can partly increase expression of EMT-related transcription factors in BT-20 and MCF-7 cells. Furthermore, EGF alone can induce a stem cell-like phenotype in BT-20 cells and promote adhesion on human umbilical vein endothelial cells (HUVECs) but cannot promote expression of EMT-related transcription factors in BT-20 cells. A combination of EGF and TGF-ß1 can promote expression of EMT-related transcription factors in BT-20 cells. 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It may not be copied or redistributed beyond the terms of applicable copyright laws."],"dc:subject":["Biomedical Engineering","Epithelial-Mesenchymal Transition","stem cell","transforming growth factor","Epidermal Growth Factor","breast cancer"],"dc:title":["Breast Cancer Cells Acquire a Stem-Like Phenotype by TGFß1/EGF Induced Epithelial-Mesenchymal Transition"],"dc:type":["Electronic Thesis or Dissertation"],"thesis:degree_discipline":["Biomedical Engineering (Engineering and Technology)"],"thesis:degree_level":["masters"],"thesis:degree_name":["Master of Science (MS)"],"thesis:institution_name":["Ohio University"]},"updated_at":"2026-07-24T03:37:46Z"}