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We aim to understand the mechanisms behind uncontrolled cell migration - which promotes progression of certain conditions - to develop new treatments to prevent this progression.

Model of MT1-MMP dimer on the cell surface MT1-MMP forms homodimer through Hpx and transmembrane domains to become a functional enzyme.
Model of MT1-MMP dimer on the cell surface MT1-MMP forms homodimer through Hpx and transmembrane domains to become a functional enzyme.

Cell migration is an essential event in our body. In normal conditions, it is precisely controlled and contributes to various aspects of a healthy system, including embryo development, wound healing and immunity.

However, when cell migration becomes uncontrolled it promotes progression of diseases such as cancer and arthritis.

Our aim is to understand key mechanisms of pathological cell migration.

When cells migrate in tissues, they need to degrade extracellular matrix (ECM) by using proteolytic enzymes to make a path, and one of the membrane-bound matrix metalloproteinases, MT1-MMP, plays a crucial role.

MT1-MMP promotes cellular invasion by degrading variety of ECM components including fibrillar collagen, by cleaving ECM receptors and by activating other MMPs. MT1-MMP is the only collagenolytic MMP that can promote cellular invasion into collagen-enriched tissues, and is implicated in various diseases including cancer and rheumatoid arthritis.

MT1-MMP not only degrade ECM components, but also various membrane proteins, which in turn modifies cell functions and promotes cellular invasion.

We are investigating the mechanisms of MT1-MMP-mediated cellular invasion in a hope to develop means to prevent progression of diseases.

Related research themes