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dc.contributor.authorJayson, Gordon C
dc.contributor.authorEvans, Gareth S
dc.contributor.authorPemberton, P W
dc.contributor.authorLobley, R W
dc.contributor.authorAllen, Terence D
dc.date.accessioned2010-04-26T09:43:17Z
dc.date.available2010-04-26T09:43:17Z
dc.date.issued1994-11-01
dc.identifier.citationBasic fibroblast growth factor increases the multiplication and migration of a serum-free derivative of CACO-2 but does not affect differentiation. 1994, 54 (21):5718-23 Cancer Res.en
dc.identifier.issn0008-5472
dc.identifier.pmid7923221
dc.identifier.urihttp://hdl.handle.net/10541/97342
dc.description.abstractBasic fibroblast growth factor (bFGF) is found in the extracellular matrix and around the endothelial and epithelial cells of some human colon carcinomas. It is believed to play a role in angiogenesis, but in addition, recent data suggest that it can directly stimulate mitogenesis in some colon carcinoma cell lines. To clarify the role of bFGF in human colon carcinoma, we developed a model of Caco-2 which grew in serum-free conditions so that the effect of bFGF on multiplication, migration, and differentiation could be studied in defined conditions. Through morphological and biochemical studies in serum-free conditions, we demonstrated that this subline of Caco-2 differentiated spontaneously on reaching confluence. Using this model, we found that bFGF did not affect differentiation but that multiplication and migration were increased. The implication of these findings is that bFGF, released from the extracellular matrix by invading cells or produced by neovascular endothelial cells, can increase the mitogenic rate and migratory potential of colon carcinoma cells. In addition, the dual role of bFGF in stimulating colon carcinoma cells directly and promoting angiogenesis suggests that anti-bFGF strategies could form the basis of a novel approach to the treatment of colon carcinoma.
dc.language.isoenen
dc.subjectColonic Canceren
dc.subjectCultured Tumour Cellsen
dc.subject.meshCell Differentiation
dc.subject.meshCell Division
dc.subject.meshCell Movement
dc.subject.meshColonic Neoplasms
dc.subject.meshCulture Media, Serum-Free
dc.subject.meshFibroblast Growth Factor 2
dc.subject.meshHumans
dc.subject.meshMicroscopy, Electron
dc.subject.meshMicroscopy, Electron, Scanning
dc.subject.meshTumor Cells, Cultured
dc.titleBasic fibroblast growth factor increases the multiplication and migration of a serum-free derivative of CACO-2 but does not affect differentiation.en
dc.typeArticleen
dc.contributor.departmentDepartment of Medical Oncology, Paterson Institute for Cancer Research, Withington, Manchester, United Kingdom.en
dc.identifier.journalCancer Researchen
html.description.abstractBasic fibroblast growth factor (bFGF) is found in the extracellular matrix and around the endothelial and epithelial cells of some human colon carcinomas. It is believed to play a role in angiogenesis, but in addition, recent data suggest that it can directly stimulate mitogenesis in some colon carcinoma cell lines. To clarify the role of bFGF in human colon carcinoma, we developed a model of Caco-2 which grew in serum-free conditions so that the effect of bFGF on multiplication, migration, and differentiation could be studied in defined conditions. Through morphological and biochemical studies in serum-free conditions, we demonstrated that this subline of Caco-2 differentiated spontaneously on reaching confluence. Using this model, we found that bFGF did not affect differentiation but that multiplication and migration were increased. The implication of these findings is that bFGF, released from the extracellular matrix by invading cells or produced by neovascular endothelial cells, can increase the mitogenic rate and migratory potential of colon carcinoma cells. In addition, the dual role of bFGF in stimulating colon carcinoma cells directly and promoting angiogenesis suggests that anti-bFGF strategies could form the basis of a novel approach to the treatment of colon carcinoma.


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