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dc.contributor.authorWalsh, Naomi*
dc.contributor.authorClynes, Martin*
dc.contributor.authorCrown, John*
dc.contributor.authorO'Donovan, Norma*
dc.date.accessioned2010-03-08T16:45:51Z
dc.date.available2010-03-08T16:45:51Z
dc.date.issued2009
dc.identifier.citationAlterations in integrin expression modulates invasion of pancreatic cancer cells. 2009, 28:140 J. Exp. Clin. Cancer Res.en
dc.identifier.issn1756-9966
dc.identifier.pmid19825166
dc.identifier.doi10.1186/1756-9966-28-140
dc.identifier.urihttp://hdl.handle.net/10147/93887
dc.description.abstractBACKGROUND: Factors mediating the invasion of pancreatic cancer cells through the extracellular matrix (ECM) are not fully understood. METHODS: In this study, sub-populations of the human pancreatic cancer cell line, MiaPaCa-2 were established which displayed differences in invasion, adhesion, anoikis, anchorage-independent growth and integrin expression. RESULTS: Clone #3 displayed higher invasion with less adhesion, while Clone #8 was less invasive with increased adhesion to ECM proteins compared to MiaPaCa-2. Clone #8 was more sensitive to anoikis than Clone #3 and MiaPaCa-2, and displayed low colony-forming efficiency in an anchorage-independent growth assay. Integrins beta 1, alpha 5 and alpha 6 were over-expressed in Clone #8. Using small interfering RNA (siRNA), integrin beta1 knockdown in Clone #8 cells increased invasion through matrigel and fibronectin, increased motility, decreased adhesion and anoikis. Integrin alpha 5 and alpha 6 knockdown also resulted in increased motility, invasion through matrigel and decreased adhesion. CONCLUSION: Our results suggest that altered expression of integrins interacting with different extracellular matrixes may play a significant role in suppressing the aggressive invasive phenotype. Analysis of these clonal populations of MiaPaCa-2 provides a model for investigations into the invasive properties of pancreatic carcinoma.
dc.language.isoenen
dc.subject.meshAnoikis
dc.subject.meshBlotting, Western
dc.subject.meshCell Adhesion
dc.subject.meshCell Line, Tumor
dc.subject.meshCell Movement
dc.subject.meshGene Expression
dc.subject.meshHumans
dc.subject.meshIntegrins
dc.subject.meshNeoplasm Invasiveness
dc.subject.meshPancreatic Neoplasms
dc.subject.meshRNA, Small Interfering
dc.subject.meshTransfection
dc.titleAlterations in integrin expression modulates invasion of pancreatic cancer cells.en
dc.contributor.departmentNational Institute for Cellular Biotechnology, Dublin City University, Glasnevin, Dublin 9, Ireland. naomi.walsh@dcu.ieen
dc.identifier.journalJournal of experimental & clinical cancer research : CRen
refterms.dateFOA2018-09-03T10:20:15Z
html.description.abstractBACKGROUND: Factors mediating the invasion of pancreatic cancer cells through the extracellular matrix (ECM) are not fully understood. METHODS: In this study, sub-populations of the human pancreatic cancer cell line, MiaPaCa-2 were established which displayed differences in invasion, adhesion, anoikis, anchorage-independent growth and integrin expression. RESULTS: Clone #3 displayed higher invasion with less adhesion, while Clone #8 was less invasive with increased adhesion to ECM proteins compared to MiaPaCa-2. Clone #8 was more sensitive to anoikis than Clone #3 and MiaPaCa-2, and displayed low colony-forming efficiency in an anchorage-independent growth assay. Integrins beta 1, alpha 5 and alpha 6 were over-expressed in Clone #8. Using small interfering RNA (siRNA), integrin beta1 knockdown in Clone #8 cells increased invasion through matrigel and fibronectin, increased motility, decreased adhesion and anoikis. Integrin alpha 5 and alpha 6 knockdown also resulted in increased motility, invasion through matrigel and decreased adhesion. CONCLUSION: Our results suggest that altered expression of integrins interacting with different extracellular matrixes may play a significant role in suppressing the aggressive invasive phenotype. Analysis of these clonal populations of MiaPaCa-2 provides a model for investigations into the invasive properties of pancreatic carcinoma.


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