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dc.contributor.authorBates, Richard C.
dc.contributor.authorMercurio, Arthur M.
dc.date2022-08-11T08:08:02.000
dc.date.accessioned2022-08-23T15:39:51Z
dc.date.available2022-08-23T15:39:51Z
dc.date.issued2005-04-23
dc.date.submitted2010-11-07
dc.identifier.citationCancer Biol Ther. 2005 Apr;4(4):365-70. Epub 2005 Apr 4.
dc.identifier.issn1538-4047 (Linking)
dc.identifier.pmid15846061
dc.identifier.urihttp://hdl.handle.net/20.500.14038/26268
dc.description.abstractDuring embryonic development, epithelial cells must escape the structural constraints imposed by tissue architecture and adopt a phenotype more amenable to cell movement, a process known as the epithelial-mesenchymal transition (EMT). The progression of carcinomas to invasive and metastatic disease may also involve localized occurrences of EMT. However, data that support the actual occurrence of EMT in specific carcinomas and the relevance of this process to the progression of these tumors had been scant. This review highlights recent studies that substantiate the importance of the EMT to colorectal carcinoma. Specifically, a novel model for studying the EMT of colorectal carcinoma has been used to gain insight into the nature of the EMT itself and to identify molecular events that contribute to disease progression. Although loss of E-cadherin function is a primal event for the EMT, the expression of specific integrins such as alpha(v)beta6 as a consequence of the EMT enables invasive cells to interact with interstitial matrices and to sustain activation of TGF-beta. Of note, alpha(v)beta6 expression in tumors is a marker of cells that have undergone an EMT and it is prognostic for tumors that will progress more rapidly to terminal disease. The EMT also induces autocrine signaling involving VEGF and Flt-1 that enable invasive cells to become 'self-sufficient' for survival. Thus, the EMT appears to be an integral component of colorectal cancer progression and its analysis can yield novel targets for prognosis and therapy.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=15846061&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.4161/cbt.4.4.1655
dc.subjectAnimals
dc.subjectAntigens, Neoplasm
dc.subjectColorectal Neoplasms
dc.subjectDisease Progression
dc.subjectEpithelium
dc.subjectHumans
dc.subjectIntegrins
dc.subjectMesoderm
dc.subjectTransforming Growth Factor beta
dc.subjectTumor Markers, Biological
dc.subjectTumor Necrosis Factor-alpha
dc.subjectVascular Endothelial Growth Factor A
dc.subjectCancer Biology
dc.subjectNeoplasms
dc.titleThe epithelial-mesenchymal transition (EMT) and colorectal cancer progression
dc.typeJournal Article
dc.source.journaltitleCancer biology and therapy
dc.source.volume4
dc.source.issue4
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/cancerbiology_pp/182
dc.identifier.contextkey1633408
html.description.abstract<p>During embryonic development, epithelial cells must escape the structural constraints imposed by tissue architecture and adopt a phenotype more amenable to cell movement, a process known as the epithelial-mesenchymal transition (EMT). The progression of carcinomas to invasive and metastatic disease may also involve localized occurrences of EMT. However, data that support the actual occurrence of EMT in specific carcinomas and the relevance of this process to the progression of these tumors had been scant. This review highlights recent studies that substantiate the importance of the EMT to colorectal carcinoma. Specifically, a novel model for studying the EMT of colorectal carcinoma has been used to gain insight into the nature of the EMT itself and to identify molecular events that contribute to disease progression. Although loss of E-cadherin function is a primal event for the EMT, the expression of specific integrins such as alpha(v)beta6 as a consequence of the EMT enables invasive cells to interact with interstitial matrices and to sustain activation of TGF-beta. Of note, alpha(v)beta6 expression in tumors is a marker of cells that have undergone an EMT and it is prognostic for tumors that will progress more rapidly to terminal disease. The EMT also induces autocrine signaling involving VEGF and Flt-1 that enable invasive cells to become 'self-sufficient' for survival. Thus, the EMT appears to be an integral component of colorectal cancer progression and its analysis can yield novel targets for prognosis and therapy.</p>
dc.identifier.submissionpathcancerbiology_pp/182
dc.contributor.departmentDepartment of Cancer Biology
dc.source.pages365-70


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