Journal
JOURNAL OF CELLULAR PHYSIOLOGY
Volume 234, Issue 3, Pages 2511-2522Publisher
WILEY
DOI: 10.1002/jcp.26783
Keywords
apoptosis; breast cancer; nuclear transcription factor-kappa B (NF-kappa B); reactive oxygen species (ROS); sodium selenite (SSE)
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Funding
- National Major Project for Breeding of Transgenic Pig [2016ZX08006-002]
- Cooperative Innovation Center for Sustainable Pig Production
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Sodium selenite (SSE), a source of inorganic selenium, has been widely used as a clinical cancer treatment, but the precise molecular mechanisms of SSE remain to be elucidated. Our in vitro experiments have confirmed that SSE treatment causes a transient increase in intracellular reactive oxygen species (ROS) levels, resulting in the inhibition of nuclear transcription factor-kappa B (NF-kappa B) signaling and p65 and nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha phosphorylation levels in 4T1 cells. The inhibition of NF-kappa B subsequently increased the expression of the apoptosis gene B-cell lymphoma-2-associated X (Bax) and downregulated the transcription of antiapoptosis genes, such as B-cell lymphoma-2, cellular inhibitor of apoptosis 1, and X-linked inhibitor of apoptosis. Additionally, the accumulation of ROS caused mitochondrial dysfunction, leading to the activation of caspase-9 and -3, thereby resulting in apoptosis. However, modulation of the ROS level by the chemical inhibitor N-acetyl-cysteine reversed these events. Similarly, in vitro murine syngeneic breast tumor models showed that SSE inhibits tumor growth by promoting apoptosis. These results indicate that SSE induces apoptosis via ROS-mediated inhibition of NF-kappa B signaling and activation of the Bax-caspase-9-caspase-3 axis.
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