Dynamin 2 (DNM2) is a large ubiquitously expressed GTPase, well known for its role in vesicle formation in endocytosis and intracellular membrane trafficking, also acting as a cytoskeletal regulator. In this review of the literature, two researchers from the Myology Centre for Research* of the Institute of Myology recall that over the past two decades, the involvement of DNM2, via mutations or overexpression, has appeared in a growing number of patients. cancers and often associated with a poor prognosis. A wide range of DNM2-dependent processes have been described in cancer cells, which explains the contribution of DNM2 to the pathological mechanisms of cancer:
- DNM2 dysfunction can promote cell migration, invasion and metastasis.
- DNM2 has an impact on intracellular signaling pathways promoting proliferation and survival of tumor cells.
In relation to these roles, DNM2 has been shown to be a capable therapeutic target, in a wide range of cancer cells in vitro:
- to reduce cell proliferation,
- to induce apoptosis
- to reduce the invasive phenotype
In addition, proof of concept for modulation therapy of DNM2 expression has also been performed in vivo in several animal models. Therefore, DNM2 appears to be a promising molecular target for the development of anti-invasive agents and the proof of concept already provided in animal models represents an important step in preclinical development.