Down-regulation of MsrB3 induces cancer cell apoptosis through reactive oxygen species production and intrinsic mitochondrial pathway activation.
作者： Geun-Hee Kwak , Tae-Hyoung Kim , Hwa-Young Kim
DOI: 10.1016/J.BBRC.2016.12.120
关键词:
摘要: Methionine sulfoxide reductase B3 (MsrB3) is a protein repair enzyme that specifically catalyzes the reduction of methionine-R-sulfoxide residues and has an antioxidant function. We have previously shown depletion MsrB3 suppresses proliferation normal mammalian cells by arresting cell cycle. In this study, we report crucial role in cancer death. Deficiency induced death, while overexpression stimulated proliferation. resulted apoptotic death through activation intrinsic mitochondrial pathway. deficiency increased levels cellular reactive oxygen species (ROS) led to redox imbalance, also Bax Bcl-2 ratio cytochrome c release, leading caspase activation. Treatment MsrB3-depleted with N-acetylcysteine, ROS scavenger, prevented suggesting deficiency-induced associated production. addition, activated poly(ADP ribose) polymerase-1 (PARP-1) translocation apoptosis-inducing factor (AIF) nucleus. Taken together, our results suggest plays important survival modulation apoptosis
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