Show simple item record

dc.contributor.authorStarobinska, Ella
dc.creatorStarobinska, Ellaen_US
dc.date.accessioned2012-09-18T20:46:42Z
dc.date.available2012-09-18T20:46:42Z
dc.date.issued2012-05
dc.identifier.urihttp://hdl.handle.net/10150/244788
dc.description.abstractIn order to metastasize, cancer cells need to invade and degrade matrix. Previous research showed that Epidermal Growth Factor Receptor (EGFR) is an oncogene, a member of ErBb family, that is over-expressed in aggressive cancers. EGFR mediates cell survival, proliferation, and motility through different signaling pathways. Located on the basolateral membrane of the cell, EGFR can be either translocated to the nucleus, degraded by the lysosome or recycled. However, in cancerous cells, EGFR activity is altered by MUC1, which associates itself with EGFR. Research suggested that this pathway acts in a Met-dependent manner. We conducted matrix degradation and invasion assays to see whether MUC1/EGFR activity has affect on these processes. Matrix degradation assay showed that Muc1 and EGFR inhibit matrix degradation and PMIP promotes it. However, Muc1/EGFR regulated matrix degradation is not Met-dependant. Meanwhile, the transwell invasion assay provided variable and statistically insignificant results.
dc.language.isoenen_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.titleMatrix Degradation and Invasion in Breast Canceren_US
dc.typetexten_US
dc.typeElectronic Thesisen_US
thesis.degree.grantorUniversity of Arizonaen_US
thesis.degree.levelbachelorsen_US
thesis.degree.disciplineHonors Collegeen_US
thesis.degree.disciplinePhysiologyen_US
thesis.degree.nameB.S.en_US
refterms.dateFOA2018-06-26T07:41:16Z
html.description.abstractIn order to metastasize, cancer cells need to invade and degrade matrix. Previous research showed that Epidermal Growth Factor Receptor (EGFR) is an oncogene, a member of ErBb family, that is over-expressed in aggressive cancers. EGFR mediates cell survival, proliferation, and motility through different signaling pathways. Located on the basolateral membrane of the cell, EGFR can be either translocated to the nucleus, degraded by the lysosome or recycled. However, in cancerous cells, EGFR activity is altered by MUC1, which associates itself with EGFR. Research suggested that this pathway acts in a Met-dependent manner. We conducted matrix degradation and invasion assays to see whether MUC1/EGFR activity has affect on these processes. Matrix degradation assay showed that Muc1 and EGFR inhibit matrix degradation and PMIP promotes it. However, Muc1/EGFR regulated matrix degradation is not Met-dependant. Meanwhile, the transwell invasion assay provided variable and statistically insignificant results.


Files in this item

Thumbnail
Name:
azu_etd_mr_2012_0178_sip1_m.pdf
Size:
750.0Kb
Format:
PDF

This item appears in the following Collection(s)

Show simple item record