Tumor-Suppressor Protein Helps Keep Breast-Cancer Protein at Bay

In Chapter 14, we have been learning about mutation, DNA repair, cancer, and the possible interconnection of the three. One of our topics was tumor-suppressor proteins, which code for proteins that fix DNA damage and down-regulate cell division, acting as inhibitors. This article talks about a protein coded for by a tumor-suppressor protein called BRCA1. This protein by keep ovarian and breast cancer at bay be preventing the transcription of repetitive DNA segments. It has long been known that there is a connection between defective BRCA1 and breast and ovarian cancer.

Researchers have been attempting to discover how BRCA1 could play a role in ceasing the cancerous activities of cells. A study was conducted by a research group on mice that lack the BRCA1 gene. They found the expected defects with DNA repair and cell cycle regulation in association with a non-functioning BRCA1 gene. In addition, they found that these cells are scarce in heterochromatic centers, which are areas of compacted, untranscribed DNA located by a chromosome's centromere. Rather, these areas were highly active and produced "satellite repeats", which are many RNA transcripts. BRCA1 proteins in normal cells keep these areas untranscribed by tagging histones with ubiquitin. When this was artificially added, the cells were able to recover.

Therefore, it was determined that BRCA1 proteins prevent genomic instability. It still remains to be discovered why BRCA1 is so specific to breast and ovarian cancer. Further research has shown that satellite repeats can be found in many types of tumor tissues, and there are most likely several factors that contribute to the inability to maintain heterochromatin. Studies also have yet to determine why people with a defective BRCA1 gene are more likely to get cancer initially, while it now know why tumors develop after BRCA1 becomes defective.