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Updated: Oct 27, 2025
CAM-Delam Assay to Score Metastatic Properties by Quantifying Delamination and Invasion Capacity of Cancer Cells
Published on: June 2, 2022
A review of Dynamin 2 involvement in cancers highlights a promising therapeutic target
Delphine Trochet1, Marc Bitoun2
1Centre de Recherche en Myologie, Sorbonne Université, Inserm, UMRS 974, Institut de Myologie, F-75013, Paris, France.
Abstract:
Dynamin 2 (DNM2) is an ubiquitously expressed large GTPase well known for its role in vesicle formation in endocytosis and intracellular membrane trafficking also acting as a regulator of cytoskeletons. During the last two decades, DNM2 involvement, through mutations or overexpression, emerged in an increasing number of cancers and often associated with poor prognosis. A wide panel of DNM2-dependent processes was described in cancer cells which explains DNM2 contribution to cancer pathomechanisms. First, DNM2 dysfunction may promote cell migration, invasion and metastasis. Second, DNM2 acts on intracellular signaling pathways fostering tumor cell proliferation and survival. Relative to these roles, DNM2 was demonstrated as a therapeutic target able to reduce cell proliferation, induce apoptosis, and reduce the invasive phenotype in a wide range of cancer cells in vitro. Moreover, proofs of concept of therapy by modulation of DNM2 expression was also achieved in vivo in several animal models. Consequently, DNM2 appears as a promising molecular target for the development of anti-invasive agents and the already provided proofs of concept in animal models represent an important step of preclinical development.
Insights
Dynamin 2 (DNM2) is implicated in cancer progression, promoting cell migration and survival. Targeting DNM2 shows promise for developing new anti-cancer therapies, with successful preclinical models established.
Area of Science:
- Molecular Biology
- Cell Biology
- Oncology
Background:
- Dynamin 2 (DNM2) is a GTPase involved in endocytosis, membrane trafficking, and cytoskeleton regulation.
- DNM2 dysfunction is increasingly linked to various cancers, often correlating with poor patient prognosis.
Purpose of the Study:
- To explore the multifaceted roles of DNM2 in cancer pathomechanisms.
- To evaluate DNM2 as a potential therapeutic target for cancer treatment.
Main Methods:
- Review of existing literature on DNM2's functions in cancer.
- Analysis of DNM2's impact on cancer cell migration, invasion, proliferation, and survival.
- Assessment of preclinical therapeutic strategies targeting DNM2.
Main Results:
- DNM2 dysfunction promotes cancer cell migration, invasion, and metastasis.
- DNM2 influences intracellular signaling pathways that enhance tumor cell proliferation and survival.
- In vitro studies demonstrate DNM2 targeting reduces cancer cell proliferation and invasiveness.
- In vivo animal models show proof-of-concept for DNM2-modulating therapies.
Conclusions:
- DNM2 is a significant contributor to cancer progression through various cellular mechanisms.
- DNM2 represents a promising molecular target for developing novel anti-invasive cancer therapies.
- Preclinical evidence supports the therapeutic potential of modulating DNM2 in cancer treatment.
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