Cell invasion through the extracellular matrix (ECM) is an important phenomenon both during normal developmental processes and cancer metastasis. When an invading cell moves through the ECM, it extends cell membrane protrusions called invadopodia into the matrix. These structures are rich in actin, actin-binding proteins as well as various proteases including MMP-9 and MMP-2 that helps the cell to degrade the matrix. Since α-catenin binds to the actin cytoskeleton either directly or indirectly via actin-binding proteins and formation of invadopodia requires the remodeling of the actin cytoskeleton, one might suspect a role of α-catenin in the biology of invadopodia formation. We have shown here that MDA-MB-468 human breast cancer cells, which do not express α-catenin form non-functional invadopodia-like structures that disassemble when full length α-catenin is overexpressed, which may be via the Erk signaling pathway. In addition, various growth factors including EGF, VEGF has been shown to induce invadopodia formation. However, the role of other growth factors, and their downstream signaling pathways on invadopodia formation have not been well studied. We have shown that TGF-β1 promotes invasive activity in human mammary epithelial cells by increasing the number of invadopodial structures. The formation of invadopodia was found to be dependent on the PI3 kinase and Src signaling pathways. In contrast, the functional activity of invadopodia to degrade the ECM was dependent on the ERK signaling pathway via the upregulation of MMP-9 expression. Furthermore, invasive cells are highly motile, and disassembly of cell-cell junctions via shedding of cadherins via the upregulation of MMPs or ADAMs further adds to their motility. However, the role of growth factors in the shedding of E-cadherin has not been fully understood and needs to be studied further. We showed that TGF-β1 induces E-cadherin shedding in CA1D cells in a dose- and time-dependent manner. In an attempt to identify the proteases involved in the shedding process, we examined MMP-3, MMP-9, ADAM-12 and ADAM-19 since their expression was transcriptionally upregulated following TGF-β1 treatment.