Breakthrough in Breast Cancer Treatment: Dimeric VIPR2 as a Promising Target

Researchers at Hiroshima University have made significant progress in understanding the molecular mechanisms behind breast cancer progression. Their recent study, published in the British Journal of Pharmacology, uncovers how the receptor molecule VIPR2 contributes to tumor growth and metastasis when overexpressed. Normally involved in regulating circadian rhythms, immune responses, and insulin secretion, VIPR2 can become excessively active in breast cancer cells.

The team focused on VIPR2's ability to form homodimers—paired receptor molecules—that enhance cancer cell proliferation. They demonstrated that these dimers are involved in tumor progression through specific binding sites on the receptor, known as transmembrane domains TM3 and 4.

By introducing peptides that disrupt this dimerization process, the researchers observed suppressed tumor growth and metastasis in cell models and mouse experiments. This de-dimerization interferes with the receptor’s signaling pathways that promote cancer cell survival and spread, offering a potential new avenue for targeted therapy.

The findings suggest that developing drugs to prevent VIPR2 dimerization might become an effective strategy to combat breast cancer, especially in cases where the receptor is overexpressed. Future studies will focus on testing the therapeutic capabilities of purified peptides like TM3-4 in animal models, with the goal of creating novel anti-cancer treatments.

This discovery provides critical insight into the molecular interactions driving breast cancer and opens promising pathways for targeted drug development, potentially improving outcomes for patients with aggressive tumors.