Assessing the role of αVβ6 in triple negative breast cancer phenotypes

Integrins are a family of heterodimeric proteins that mediates cell adhesion, polarity and signaling. The integrin αVβ6, is typically expressed during physiological processes such as embryogenesis, and fibrosis. Aberrant expression is associated with different types of cancer and metastasis with higher expression correlating to poor prognosis in patients. In order to understand the role of αVβ6 integrin in breast cancer and how it can mediate cancer specific phenotypes, research was conducted on triple negative breast cancer cell lines (TNBC), a particularly aggressive cancer subtype. TNBC cell lines MDA-MB-468 (αVβ6+) and MDA-MB-231 (αVβ6-) were used as models to study αVβ6 mediated phenotypes. Inducing the expression of αVβ6 in MDA-MB-231 cells helped determine whether it was sufficient for cancer phenotypes like enhanced adhesion, migration, proliferation and expression of EMT markers; while silencing it in MDA-MB-468 facilitated the study of whether it was required for these phenotypes. Adhesion on the latency associated peptide containing TGFβ-1 (LAP-TGFβ-1) was used to study the effects of the integrin αVβ6 on cellular adhesion. While αVβ6 is required for adhesion in MDAMB468 cells, it is not sufficient in MDAMB231 cells. Inducing the overexpression of αVβ6 in MDA-MB-231 seems to result in a decrease in proliferation, while silencing it enhances proliferation. This negative regulation was also seen in the expression of the EMT marker vimentin while no change in E-cadherin was observed. αVβ6 is required for migration in MDAMB468 cells as a decrease was observed following knockdown.