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Sodium selenite induces apoptosis via ROS‐mediated NF‐κB signaling and activation of the Bax–caspase‐9–caspase‐3 axis in 4T1 cells

Tao Zhang,Gan Zhao,Xinying Zhu,Kangfeng Jiang,Haichong Wu,Ganzhen Deng,Changwei Qiu

Published 2018 in Journal of Cellular Physiology

ABSTRACT

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‐κB (NF‐κB) 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‐κB 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‐κB signaling and activation of the Bax–caspase‐9–caspase‐3 axis.

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