A research group including Assistant Professor Satoshi Asano and Professor Yukio Ago of Hiroshima University and Professor Takanobu Nakazawa of Tokyo University of Agriculture has revealed that dimerization of the neuropeptide receptor VIPR2 is a factor in the proliferation and metastasis of breast cancer.
This group has previously found that the number of copies of the gene for a neuropeptide receptor called VIPR2 and the expression of mRNA, which is the blueprint for creating VIPR2, are increased in breast cancer. VIPR2 improves blood flow, promotes digestion, and regulates stress by binding to specific neuropeptides, but it has also recently been revealed that it is an important molecule that controls cell proliferation and migration in breast cancer.
This time, the research group discovered that VIPR2 forms a dimer in breast cancer cells. They also found that the transmembrane domains 3-4 of the cell membrane are essential for dimerization, and succeeded in inhibiting dimerization by overexpressing the transmembrane domains 3-4 in cancer cells using the competitive binding property of the transmembrane domain 3-4 peptide.
Furthermore, they established a breast cancer cell line expressing transmembrane domains 3-4, and found that transplanting this into mice suppressed the proliferation and metastasis of breast cancer cells in the mice. This suggests that dimeric VIPR2 is a molecule that aggravates breast cancer, and that inhibiting dimerization may significantly suppress cancer growth and metastasis.
In the future, to explore the possibility that the transmembrane domain 2-3 peptide that inhibits VIPR4 dimerization could be a candidate for a new anticancer drug, the researchers plan to verify the anticancer effect of the transmembrane domain 2-3 peptide targeting cancer cells with enhanced VIPR4 dimerization using animal models. It is hoped that a new drug that can halt the progression of breast cancer by preventing VIPR2 dimerization can be developed.
