The research on “BRCA1 Overexpression via the NRF2/HO1/NQO1 Pathway on Oral Cancer Cells Proliferation, Migration, and Apoptosis” sheds light on the role of the BRCA1 gene, a well-known tumor suppressor, in the context of oral cancer. BRCA1 is traditionally associated with breast and ovarian cancers, where its loss of function due to mutations leads to increased genomic instability and cancer susceptibility. This study investigates the effects of BRCA1 overexpression, rather than loss, that might be addressed also in oral squamous cell carcinoma (OSCC) cells.

By transfecting OSCC cells with a lentivirus carrying the BRCA1 gene, the researchers observed that overexpression of BRCA1 led to a significant reduction in cell proliferation and migration, while promoting apoptosis. These effects were mediated through the NRF2/HO1/NQO1 pathway, a key regulator of cellular antioxidant defenses. The upregulation of this pathway in response to BRCA1 overexpression suggests that BRCA1 may enhance the cellular response to oxidative stress, thereby inhibiting cancer cell survival.

This study highlights the complexity of BRCA1’s role in cancer biology, as its overexpression can have tumor-suppressive effects in certain contexts. The findings suggest that BRCA1-based gene therapy could be a potential strategy for treating OSCC, particularly in cases where the cancer cells exhibit heightened oxidative stress.

However, the therapeutic implications of these findings are complicated by the fact that BRCA1’s effects can vary depending on the type of cancer and its molecular context. Further research is needed to determine whether BRCA1 overexpression could be beneficial in other cancer types and to assess the safety of BRCA1-based gene therapies in clinical trials.