Breast cancer growth and metastasis: interplay between cancer stem cells, embryonic signaling pathways and epithelial-to-mesenchymal transition
Induction of epithelial-to-mesenchymal transition (EMT) in cancer stem cells (CSCs) can occur as the result of embryonic pathway signaling. Activation of Hedgehog (Hh), Wnt, Notch, or transforming growth factor-β leads to the upregulation of a group of transcriptional factors that drive EMT. This pr...
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Veröffentlicht in: | Breast cancer research : BCR 2011-06, Vol.13 (3), p.211-211, Article 211 |
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description | Induction of epithelial-to-mesenchymal transition (EMT) in cancer stem cells (CSCs) can occur as the result of embryonic pathway signaling. Activation of Hedgehog (Hh), Wnt, Notch, or transforming growth factor-β leads to the upregulation of a group of transcriptional factors that drive EMT. This process leads to the transformation of adhesive, non-mobile, epithelial-like tumor cells into cells with a mobile, invasive phenotype. CSCs and the EMT process are currently being investigated for the role they play in driving metastatic tumor formation in breast cancer. Both are very closely associated with embryonic signaling pathways that stimulate self-renewal properties of CSCs and EMT-inducing transcription factors. Understanding these mechanisms and embryonic signaling pathways may lead to new opportunities for developing therapeutic agents to help prevent metastasis in breast cancer. In this review, we examine embryonic signaling pathways, CSCs, and factors affecting EMT. |
doi_str_mv | 10.1186/bcr2876 |
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Activation of Hedgehog (Hh), Wnt, Notch, or transforming growth factor-β leads to the upregulation of a group of transcriptional factors that drive EMT. This process leads to the transformation of adhesive, non-mobile, epithelial-like tumor cells into cells with a mobile, invasive phenotype. CSCs and the EMT process are currently being investigated for the role they play in driving metastatic tumor formation in breast cancer. Both are very closely associated with embryonic signaling pathways that stimulate self-renewal properties of CSCs and EMT-inducing transcription factors. Understanding these mechanisms and embryonic signaling pathways may lead to new opportunities for developing therapeutic agents to help prevent metastasis in breast cancer. 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Activation of Hedgehog (Hh), Wnt, Notch, or transforming growth factor-β leads to the upregulation of a group of transcriptional factors that drive EMT. This process leads to the transformation of adhesive, non-mobile, epithelial-like tumor cells into cells with a mobile, invasive phenotype. CSCs and the EMT process are currently being investigated for the role they play in driving metastatic tumor formation in breast cancer. Both are very closely associated with embryonic signaling pathways that stimulate self-renewal properties of CSCs and EMT-inducing transcription factors. Understanding these mechanisms and embryonic signaling pathways may lead to new opportunities for developing therapeutic agents to help prevent metastasis in breast cancer. In this review, we examine embryonic signaling pathways, CSCs, and factors affecting EMT.</description><subject>Animals</subject><subject>Bone morphogenetic proteins</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cancer metastasis</subject><subject>Cancer prevention</subject><subject>DNA binding proteins</subject><subject>Epithelial-Mesenchymal Transition</subject><subject>Female</subject><subject>Growth</subject><subject>Hedgehog Proteins - metabolism</subject><subject>Humans</subject><subject>Mice</subject><subject>Neoplasm Metastasis</subject><subject>Neoplastic Stem Cells - metabolism</subject><subject>Neoplastic Stem Cells - pathology</subject><subject>Receptors, Notch - metabolism</subject><subject>Review</subject><subject>Signal Transduction</subject><subject>Transforming Growth Factor beta - metabolism</subject><subject>Wnt Signaling Pathway</subject><issn>1465-542X</issn><issn>1465-5411</issn><issn>1465-542X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kl2L1TAQhoso7rqK_0ACXnhj1yZpT9u9ENbFL1jwRsG7MEmnbSQfNcnx0F_hX7b1nF3OASUXCZl3nnkzmSx7TotLSpvNG6kCa-rNg-yclpsqr0r2_eHR-Sx7EuOPoqB1UzWPszNGNzVjDTvPfr8LCDERBU5hIEPwuzQScB2xmJYARB2viHYJw2RgJhLTDtHd6WNCSxQaE18TtDLM3mlFoh4cGO0GMkEadzDHv0ScdBrRaDB58rnFiE6NswVDUgAXddLePc0e9WAiPjvsF9m3D--_3nzKb798_HxzfZvLqmIpbxWlsuPIuqYHYJQXvC24anu5dKNlKKlq666ErkbsK86oBK7Kvq_aFkoOnF9kb_fcaSstdgrd4sGIKWgLYRYetDiNOD2Kwf8SC6tp-Qq42gOk9v8BnEaUt-LwTUvyq0P14H9uMSZhdVzbCA79Noq2qJp6edWqfLlXDmBQaNf7BaZWtbgu66ZkZdmsZi7_oVpWh1Yr77DXy_1JwsGACj7GgP29cVqIdaKOrL44btS97m6E-B8X2Myh</recordid><startdate>20110610</startdate><enddate>20110610</enddate><creator>Takebe, Naoko</creator><creator>Warren, Ronald Q</creator><creator>Ivy, S Percy</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20110610</creationdate><title>Breast cancer growth and metastasis: interplay between cancer stem cells, embryonic signaling pathways and epithelial-to-mesenchymal transition</title><author>Takebe, Naoko ; Warren, Ronald Q ; Ivy, S Percy</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b552t-9c11bd3e2d8faa21303903c9fb18692eb1c97d4ad7eef5321ba3c4ff599a43a33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Bone morphogenetic proteins</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Cancer metastasis</topic><topic>Cancer prevention</topic><topic>DNA binding proteins</topic><topic>Epithelial-Mesenchymal Transition</topic><topic>Female</topic><topic>Growth</topic><topic>Hedgehog Proteins - metabolism</topic><topic>Humans</topic><topic>Mice</topic><topic>Neoplasm Metastasis</topic><topic>Neoplastic Stem Cells - metabolism</topic><topic>Neoplastic Stem Cells - pathology</topic><topic>Receptors, Notch - metabolism</topic><topic>Review</topic><topic>Signal Transduction</topic><topic>Transforming Growth Factor beta - metabolism</topic><topic>Wnt Signaling Pathway</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Takebe, Naoko</creatorcontrib><creatorcontrib>Warren, Ronald Q</creatorcontrib><creatorcontrib>Ivy, S Percy</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Breast cancer research : BCR</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Takebe, Naoko</au><au>Warren, Ronald Q</au><au>Ivy, S Percy</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Breast cancer growth and metastasis: interplay between cancer stem cells, embryonic signaling pathways and epithelial-to-mesenchymal transition</atitle><jtitle>Breast cancer research : BCR</jtitle><addtitle>Breast Cancer Res</addtitle><date>2011-06-10</date><risdate>2011</risdate><volume>13</volume><issue>3</issue><spage>211</spage><epage>211</epage><pages>211-211</pages><artnum>211</artnum><issn>1465-542X</issn><issn>1465-5411</issn><eissn>1465-542X</eissn><abstract>Induction of epithelial-to-mesenchymal transition (EMT) in cancer stem cells (CSCs) can occur as the result of embryonic pathway signaling. Activation of Hedgehog (Hh), Wnt, Notch, or transforming growth factor-β leads to the upregulation of a group of transcriptional factors that drive EMT. This process leads to the transformation of adhesive, non-mobile, epithelial-like tumor cells into cells with a mobile, invasive phenotype. CSCs and the EMT process are currently being investigated for the role they play in driving metastatic tumor formation in breast cancer. Both are very closely associated with embryonic signaling pathways that stimulate self-renewal properties of CSCs and EMT-inducing transcription factors. Understanding these mechanisms and embryonic signaling pathways may lead to new opportunities for developing therapeutic agents to help prevent metastasis in breast cancer. In this review, we examine embryonic signaling pathways, CSCs, and factors affecting EMT.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>21672282</pmid><doi>10.1186/bcr2876</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Bone morphogenetic proteins Breast cancer Breast Neoplasms - metabolism Breast Neoplasms - pathology Cancer metastasis Cancer prevention DNA binding proteins Epithelial-Mesenchymal Transition Female Growth Hedgehog Proteins - metabolism Humans Mice Neoplasm Metastasis Neoplastic Stem Cells - metabolism Neoplastic Stem Cells - pathology Receptors, Notch - metabolism Review Signal Transduction Transforming Growth Factor beta - metabolism Wnt Signaling Pathway |
title | Breast cancer growth and metastasis: interplay between cancer stem cells, embryonic signaling pathways and epithelial-to-mesenchymal transition |
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