Breast cancer susceptibility protein 1 (BRCA1) and its heterodimeric partner BARD1 play an essential role in genomic stability by regulating DNA damage repair, cell-cycle checkpoints, and transcription regulation. Germline mutation in either of these genes exposes individuals to a higher risk of developing breast and ovarian cancer. The Caenorhabditis elegans orthologs,
brc-1 and
brd-1, also regulate DNA damage repair and cell cycle checkpoints; however, their role in regulating gene transcription is still unknown. Here, we show the transcriptional regulation function of
brc-1 and
brd-1 is conserved in worms using the
cyp-13A subfamily of genes, which are the homolog of a human estrogen metabolizing gene CYP3A4. Using gene expression analysis, we found that knocking out
brc-1 resulted in significant upregulation of four
cyp-13A subfamily of genes, and loss of
brd-1 function led to upregulation of six
cyp-13A subfamily of genes. Our finding provides insights into how
brc-1/brd-1 transcriptional regulation function is conserved in worms and further validates using C. elegans as a model system to investigate BRCA1 functions.