In vitro analysis of the invasive phenotype of SUM 149, an inflammatory breast cancer cell line

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dc.creatorHoffmeyer, Michaela R.en
dc.creatorWall, Kristin M.en
dc.creatorDharmawardhane, Suranganie F.en
dc.date.accessioned2014-12-15T17:10:32Zen
dc.date.available2014-12-15T17:10:32Zen
dc.date.issued2005-04-27en
dc.descriptionMichaela R. Hoffmeyer and Suranganie F. Dharmawatdhane are with the Department of Molecular Cell and Developmental Biology, University of Texas Austin Austin, Texas USA -- Kristin M. Wall is with the Department of Biomedical Engineering, University of Texas at Austin, AustinTX USAen
dc.description.abstractBackground: Inflammatory breast cancer (IBC) is the most lethal form of locally invasive breast cancer known. However, very little information is available on the cellular mechanisms responsible for manifestation of the IBC phenotype. To understand the unique phenotype of IBC, we compared the motile and adhesive interactions of an IBC cell line, SUM 149, to the non-IBC cell line SUM 102. -- Results: Our results demonstrate that both IBC and non-IBC cell lines exhibit similar adhesive properties to basal lamina, but SUM 149 showed a marked increase in adhesion to collagen I. In vitro haptotaxis assays demonstrate that SUM 149 was less invasive, while wound healing assays show a less in vitro migratory phenotype for SUM 149 cells relative to SUM 102 cells. We also demonstrate a role for Rho and E-cadherin in the unique invasive phenotype of IBC. Immunoblotting reveals higher E-cadherin and RhoA expression in the IBC cell line but similar RhoC expression. Rhodamine phalloidin staining demonstrates increased formation of actin stress fibers and larger focal adhesions in SUM 149 relative to the SUM 102 cell line. -- Conclusion: The observed unique actin and cellular architecture as well as the invasive and adhesive responses to the extracellular matrix of SUM 149 IBC cells suggest that the preference of IBC cells for connective tissue, possibly a mediator important for the vasculogenic mimicry via tubulogenesis seen in IBC pathological specimens. Overexpression of E-cadherin and RhoA may contribute to passive dissemination of IBC by promoting cell-cell adhesion and actin cytoskeletal structures that maintain tissue integrity. Therefore, we believe that these findings indicate a passive metastatic mechanism by which IBC cells invade the circulatory system as tumor emboli rather than by active migratory mechanisms.en
dc.description.catalogingnotesurangi@mail.utexas.eduen
dc.description.departmentBiomedical Engineeringen
dc.description.sponsorshipen
dc.identifier.Filename1475-2867-5-11en
dc.identifier.citationHoffmeyer, Michaela R., Kristin M. Wall, and Suranganie F. Dharmawardhane. “In Vitro Analysis of the Invasive Phenotype of SUM 149, an Inflammatory Breast Cancer Cell Line.” Cancer Cell International 5, no. 1 (April 27, 2005): 11. doi:10.1186/1475-2867-5-11.en
dc.identifier.doidoi:10.1186/1475-2867-5-11en
dc.identifier.urihttp://hdl.handle.net/2152/27897en
dc.language.isoEnglishen
dc.publisherCancer Cell Internationalen
dc.rightsAdministrative deposit of works to UT Digital Repository: This works author(s) is or was a University faculty member, student or staff member; this article is already available through open access at http://www.biomedcentral.com. The public license is specified as CC-BY: http://creativecommons.org/licenses/by/4.0/. The library makes the deposit as a matter of fair use (for scholarly, educational, and research purposes), and to preserve the work and further secure public access to the works of the University.en
dc.subjectinvasive phenotypeen
dc.subjectSUM 149en
dc.subjectinflammatory breast cancer cellen
dc.titleIn vitro analysis of the invasive phenotype of SUM 149, an inflammatory breast cancer cell lineen
dc.typeArticleen

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