Sodium Selenite Induces Apoptosis in Acute Promyelocytic Leukemia-Derived NB4 Cells Through Mitochondria-Dependent Pathway

Abstract

Our previous study has shown that sodium selenite can cause apoptosis in acute promyelocytic leukemia-derived NB4 cells in a caspase-dependent manner involving Deltapsim disruption and cleavage of Bcl-2, but more detailed mechanism(s) remain unclear. Here we showed that mitochondrial apoptosis signaling pathway played a vital role in apoptosis induced by sodium selenite based on the following findings: 1) cytochrome c release, activation of caspase 9, mitochondrial targeting, and oligermerization of Bax; 2) caspase 9, but not caspase 8, inhibitor could attenuate apoptosis; 3) downregulation of Bax and Bad by siRNA could delay sodium selenite-induced apoptosis. Further investigation showed that ROS was an essential inducer of deltapsim disruption and apoptosis by sodium selenite. Our findings here demonstrate that sodium selenite can induce apoptosis in NB4 cells through a mechanism involving ROS, activation of proapoptotic proteins Bad and Bax, Deltapsim disruption, release of cytochrome c, and consequent initiation of caspase cascade.

The p38 MAPK-regulated PKD1/CREB/Bcl-2 pathway contributes to selenite-induced colorectal cancer cell apoptosis in vitro and in vivo

“…Bcl-2 family proteins are essential regulators of selenite-induced apoptosis [23][24][25]. The cells were exposed to 10 μM selenite for 24 h, and co-immunoprecipitation was used to detect the interactions between PKD1 and CREB.…”

Nano - drug delivery of apoptosis activator 2 to AGS cells by liposomes conjugated with anti-TROP2 antibody

“…Also, TUNEL test in AGS cells treated with 10 μM of apoptosis activator 2/ml of RPMI 1640 culture media supplemented with 1% of BSA showed a significant increase in apoptosis in comparison with non-treated AGS cells and selenite sodium control concentration (2.5 and 4 mM) which causes necrosis instead of apoptosis as seen in AGS cells[23] [Figure 2]. …”

“…Analysis of apoptosis by Quantify Nucleosomes in cell cultures with the cell death detection ELISA showed that AGS cells treated with 10 μM of apoptosis activate 2/ml of RPMI 1640 culture media supplemented with 1% of BSA showed a significant increase in apoptosis in comparison with non-treated AGS cells. Also, in this experiment, cytotoxic concentrations (2.5 and 4 mM) of selenite sodium were used as control of cell death by necrosis[23] [Figure 3]. …”

Selenite‐Releasing Bone Mineral Nanoparticles Retard Bone Tumor Growth and Improve Healthy Tissue Functions In Vivo

“…These results, along with those obtained from selenite release profiles in PBS solution (Figure ), indicated that HANSe3 materials could be degraded in the tumor tissue and then release selenite ions, which further inhibited tumor growth. Indeed, selenite ions could inhibit cancer cell growth by inducing apoptosis …”