Elucidation of a new DNA repair mechanism, which promotes mammary tumorigenesis

 A research group headed by Professor Akira Nakai and Associate Professor Mitsuaki Fujimoto at Yamaguchi University Graduate School of Medicine (Biochemistry Course), has discovered a "new protein complex" that supports the functioning of the DNA repair mechanisms and promotes the progression of cancer. The discovery is the first of its kind in the world, and was made through collaboration with Professor Katsuhiko Shirahige and colleagues at the University of Tokyo Institute of Molecular and Cellular Biosciences.

DNA, which is the genetic information for the cells in our bodies, unceasingly receives a variety of damage, but at the same time, it maintains stability thanks to a number of repair mechanisms. However, if DNA becomes unstable and abnormalities accumulate, cancer develops. The subsequent progression of the cancer is supported by the functioning of the DNA repair mechanisms.

The BRCA1 gene is the gene that is best known as one that is related to breast cancer. In the research by Professor Nakai et al., this "new protein complex" significantly promoted breast cancer cell growth and tumorigenesis in mice with a mutated BRCA1 gene. Furthermore, it was also clarified that under conditions in which this "new protein complex" is not formed, breast cancer cell growth and tumorigenesis are significantly suppressed.

The discovered "new protein complex" shows the possibility that, by finding a compound that blocks the complex formation, it could become a target for treatment of breast cancer with fewer side effects. It is anticipated that the "new protein complex" will be used in the development of cancer drugs, etc.

This research was conducted as a part of research for the "Translation Research Center for Refractory Diseases" at Yamaguchi University Research Center for Advanced Science and Innovation (representative: Professor Akira Nakai), and published in the electronic version of the British science journal Nature Communications on Tuesday, November 21 (DOI: 10.1038/s41467-017-01807-7).