ECM effects on integrin-mediated signaling in breast cancer cells

Integrins are heterodimeric transmembrane proteins that change the intracellular pathways and signaling based on changes in the extracellular matrix (ECM)[1]. Integrins are heterodimeric adhesion receptors responsible for attachment and migration of adherent cells. In addition, integrins are signaling receptors capable of transducing signals in cells. Integrins-mediated adhesion and signaling can control different cell processes and behaviors such as cell’s  migration, adhesion, differentiation, ability to survive and more. Different integrins and the presence of different ECM proteins can transduce different signaling in adherent cells. The relevance of the project is to investigate the specific effect of ECM proteins on cell signaling. The research question is whether exposing breast cancer cells to different ECM proteins can change their signaling. To investigate this question, the cell lines used are MDA-MB-468 and MCF7. MDA-MB-468 cells are epithelial, human breast cancer cells that are invasive and differentiated triple-negative[2][3]. The MCF7 cells are also epithelial, human breast cancer cells[4] but are non-invasive and non-metastatic. The MCF7 cell-line would be used as a control. By using the 2 cell lines, we can link the different cells’ behaviors to specific ECM-mediated signaling. The methods used are cell culture, cell-adhesion assay and Western blot. The specific matrices used in the cell adhesion assay would be fibronectin, fibrinogen, collagen, BSA and serum. The signaling in the cells would be compared in different ECM proteins. Moreover, the same cell line would be exposed to different ECM proteins and test for different signaling. The Western blot analysis would provide data about the phosphorylation of the following kinases: AKT, p38, ERK and FAK. These kinases would be targeted using antibodies against them. The Western blot analysis would inform about differences in the 2 cell lines that affect different behavior.

 

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  • Author

    Sondoss Hassan

  • Advisor

    Mohamed Bouaouina

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