The study, published in the British Journal of Pharmacology, demonstrated that VIPR2 homodimerization plays a crucial role in breast cancer cell proliferation and metastasis.

VIPR2 is a receptor that can be overexpressed in breast cancer, leading to increased tumor growth and metastasis by forming dimers when VIPR2 molecules bind together.

The researchers established that VIPR2 monomers interact to form dimers through transmembrane domains, which can either promote or inhibit dimerization depending on the presence of specific protein chains known as TM3-4 peptides.

These TM3-4 peptides disrupt the interaction between VIPR2 molecules, leading to de-dimerization, which subsequently reduced cell proliferation and metastasis in breast cancer models.

By causing VIPR2 to de-dimerize, TM3-4 decreased its interaction with specific proteins and inhibited signaling pathways associated with cell proliferation and metastasis.

The findings suggest that the TM3-4 peptide could be developed into a novel anticancer drug aimed at inhibiting the harmful effects of VIPR2 overexpression.

The researchers aim to further investigate the anticancer effects of the purified TM3-4 peptide in animal models, with the goal of developing novel anticancer drugs targeting overexpressed VIPR2 in cancer cells.

The study was conducted by a team including co-corresponding authors Satoshi Asano and Yukio Ago, who are affiliated with Hiroshima University's Graduate School of Biomedical and Health Sciences and School of Dentistry.

The research was supported by multiple funding sources, including the Japan Society for the Promotion of Science and the Hiroshima University Fund 'Nozomi H Foundation.'

The study was also supported by the Japan Agency for Medical Research and Development.

The research team demonstrated that VIPR2 homodimerizes and plays a role in breast tumor growth and metastasis.

Researchers at Hiroshima University have identified a potential new anticancer drug targeting breast cancer cells by focusing on the vasoactive intestinal peptide receptor-2 (VIPR2).