Conclusions
Experiments involving oral cancer cells confirmed that BRCA1 overexpression could up-regulate the NRF2 signalling pathway, reduce oxidative damage, and inhibit cell proliferation and other biological behaviours. The BRCA1 and NRF2 pathways might be associated with oral cancer occurrence and development.
Objective
Herein, we explored the influences of breast cancer susceptibility gene 1 (BRCA1) overexpression on oral cancer cells proliferation, migration, and apoptosis via evaluation of its interactions with nuclear factor erythroid 2-like 2 (NRF2). Design: CAL-27 and DOK cells were transfected with a BRCA1 overexpressing lentivirus. Next, we utilized Western blot and quantitative real-time polymerase chain reaction (qRT-PCR) analyses to evaluate BRCA1, NRF2, and their target gene expressions. Using cell counting kit-8 (CCK-8) assessment, we assessed cell proliferation and a scratch test detected CAL-27 cell migration. Additionally, flow cytometry was employed used to examine cell apoptosis, while an enzyme-linked immunosorbent assa (ELISA) was employed for evaluation of 8-hydroxy-2'- deoxyguanosine (8-OHdG) expression. An immunohistochemical analysis was employed to determine the NRF2 target genes and Ki-67 expressions.
Results
BRCA1 overexpression increased the NRF2 and its target gene transcript and protein expressions. CCK-8 and scratch test results showed that BRCA1 overexpression decreased cell proliferation and weakened CAL-27 cell migratory ability. Flow cytometry results showed that BRCA1 overexpression promoted cell apoptosis in a time-dependent manner, while enzyme-linked immunosorbent assay results showed that BRCA1 overexpression decreased 8-OHdG expression levels in CAL-27 and DOK cells. Immunohistochemical analysis results showed higher expression of NRF2 target genes and Ki-67 in oral squamous cell carcinoma cells. Conclusions: Experiments involving oral cancer cells confirmed that BRCA1 overexpression could up-regulate the NRF2 signalling pathway, reduce oxidative damage, and inhibit cell proliferation and other biological behaviours. The BRCA1 and NRF2 pathways might be associated with oral cancer occurrence and development.