🔬 Discovery of a mechanism driving breast cancer metastases

How to explain that breast cancer cells manage to evade therapies and spread throughout the body? This question mobilizes many researchers, and a serious lead seems to involve a cellular receptor.

Named VIPR2, this receptor normally helps regulate our daily rhythm and our immune defenses. It also participates in the release of insulin, involved in fundamental biological functions. While its standard activity is beneficial, a malfunction can lead to significant effects.


When cells produce an excessive amount of VIPR2, this overexpression can accelerate the proliferation of cancer cells. In overabundance, the receptor then tends to associate with an identical copy of itself. This association forms a structure called a dimer, which alters its cellular behavior.

To explore this mechanism in detail, a team from Hiroshima University conducted a series of investigations. Their work, published in the British Journal of Pharmacology, indicates that the dimerization of VIPR2 plays a major role in tumor progression and the appearance of metastases. Experiments on cells and murine models have confirmed this influence.

These advances could lead to innovative drugs specifically targeting cells where VIPR2 dimerization is amplified. By clarifying these molecular interactions, the research offers a glimmer of hope for more refined therapies against breast cancer.