A new study led by The University of Texas Health Science Center at San Antonio (UT Health San Antonio) is shedding light on a novel role of breast cancer gene 1 (BRCA1) in tumor suppression.
Individuals with inherited mutations in BRCA1 are predisposed to breast, ovarian and other cancers. BRCA1 helps prevent cancer by repairing damaged DNA, but how it does so remains to be determined. The damage in question is the DNA double-strand break, where both strands of DNA are broken and can lead to cancer if not repaired or if repaired inaccurately. The new research led by UT Health San Antonio shows that BRCA1 not only pushes a DNA break toward an accurate DNA repair mechanism called homologous recombination (HR) but also promotes subsequent steps by spurring the activity of “end resection enzymes” that process DNA ends to prepare them for HR. “Our biochemical analysis with purified BRCA1 protein helps illuminate its role in DNA end processing,” said Patrick Sung, DPhil, associate dean for research at UT Health San Antonio and director of its Greehey Children’s Cancer Research Institute. He is a senior author of the new study titled, “Promotion of DNA end resection by BRCA1-BARD1 in homologous recombination,” published Sept. 11 in the journal Nature. “This study helps us understand why BRCA1 is such an important tumor suppressor, as it really plays more than one critical role in HR,” said Sandeep Burma, PhD, professor and vice chair (research) of neurosurgery at UT Health San Antonio and its Mays Cancer Center. He is a senior and co-communicating author of the study.
