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Specifically, overexpressed GPX3 induced mitochondrial dysfunction and cytoplasmic transfer of Cyto-C through up-regulation of BAX and down-regulation of Bcl-2, and ultimately induced mitochondria-dependent apoptosis via the caspase 9-caspase 3 cascade, and then cooperated with the blocking effect of GPX3 on G0/G1 phase to attenuate the proliferation activity of prostate cells

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