TL;DRAbstract
Tumor cell migration is a complex phenotype mediated by the genetic characteristics of the tumor cells in cooperation with the microenvironment. ADAM9, a member of a family of transmembrane matrix-metalloproteases, is implicated in cell-cell and cell-matrix interactions and the shedding of membrane receptors and ligands. ADAM9 is expressed as two alternatively spliced isoforms—membrane tethered ADAM9-Long (ADAM9-L) and secreted ADAM9-Short (ADAM9-S). ADAM9-L expression is observed in multiple epithelial cancers, while stromal cells in both the liver and bone secrete ADAM9-S. Expression of ADAM9-S increases breast cancer cell invasion, leading to the hypothesis that ADAM9 isoforms in breast tumors mediate tumor cell migration. To evaluate the hypothesis that ADAM9-isoforms are functionally relevant for breast cancer progression, I first evaluated the expression of ADAM9 isoforms in breast cancer cell lines and tissues. Characterization of an ADAM9-S specific antibody allowed for the fir
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Tumor cell migration is a complex phenotype mediated by the genetic characteristics of the tumor cells in cooperation with the microenvironment. ADAM9, a member of a family of transmembrane matrix-metalloproteases, is implicated in cell-cell and cell-matrix interactions and the shedding of membrane receptors and ligands. ADAM9 is expressed as two alternatively spliced isoforms—membrane tethered ADAM9-Long (ADAM9-L) and secreted ADAM9-Short (ADAM9-S). ADAM9-L expression is observed in multiple epithelial cancers, while stromal cells in both the liver and bone secrete ADAM9-S. Expression of ADAM9-S increases breast cancer cell invasion, leading to the hypothesis that ADAM9 isoforms in breast tumors mediate tumor cell migration. To evaluate the hypothesis that ADAM9-isoforms are functionally relevant for breast cancer progression, I first evaluated the expression of ADAM9 isoforms in breast cancer cell lines and tissues. Characterization of an ADAM9-S specific antibody allowed for the fir
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