Advances in missing-in-metastasis research

Abstract

Missing-in-metastasis (MIM, also known as metastasis suppressor 1) belongs to the inverse BAR (I-BAR) family of intracellular membrane remodeling proteins. Structurally, MIM displays typical I-BAR family protein features including the ability to dimerize through its N-terminal I-BAR domain, which can be arrested by specific peptide inhibitors. It also induces filopodia-like membrane protrusions, and can reform artificial phospholipid vesicles. MIM binds to the inner plasma membrane and participates in multiple cellular activities including cell polarization, mobility, actin cytoskeleton regulation, protein interaction, cellular signal pathway facilitation, membrane shaping, and endocytosis. These activities are mostly performed in the nervous, circulatory, urinary, and reproductive systems. MIM abnormalities occur in a number of human diseases, especially those involving tumor genesis and metastasis. As well as MIM-specific peptides, RNA interference can be used to inhibit MIM expression. These molecular tools have the potential to be used in future bio-pharmaceutical developments. In this review, advances in MIM-related research are summarized, and the prospect of MIM targeting therapy and other MIM-based applications are introduced.