2-Benzoyloxycinnamaldehyde (BCA) is a promising antitumor agent which induces cancer cells apoptosis
via reactive oxygen species (ROS) generation. BCA shows more effective antiproliferation in MDAMB-
435 than in MCF-7 breast cancer cells. DJ-1 has been known to protect cells against oxidative stress as
an antioxidant because of its cysteine residues sensitive to oxidative stress. In the present study, we evaluated
the mechanism of DJ-1 for cell protection from oxidative stress after BCA treatment in MCF-7 cell. BCA
upregulates the expression of DJ-1 in MCF-7 cells. However, DJ-1 expression decreased continuously for 24 h
after BCA treatment in MDA-MB-435 cells. DJ-1 knockdown sensitized MCF-7 cells to BCA, on the contrary,
DJ-1 overexpression induced MDA-MB-435 cells less sensitive to BCA. Confocal microscopic observation
showed that only in MCF-7 cells BCA increased the overlapped signal between mitochondria and DJ-1
protein. Mitochondrial membrane potential (MMP) was decreased in MDA-MB-435 cells by BCA, and DJ-1
overexpression inhibited BCA-induced MMP decrease in these cells. On the contrary, DJ-1 knockdown in
MCF-7 induced MMP perturbation by BCA. These findings suggest that DJ-1 upregulation protects MCF-7
cells from BCA via inhibiting mitochondrial damage.