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      Downregulation of protein kinase Cα was involved in selenite-induced apoptosis of NB4 cells.

      Oncology research
      Antineoplastic Agents, pharmacology, Apoptosis, drug effects, Caspase 3, physiology, Cell Line, Tumor, Down-Regulation, Extracellular Signal-Regulated MAP Kinases, metabolism, Humans, Leukemia, Promyelocytic, Acute, drug therapy, pathology, Protein Kinase C-alpha, antagonists & inhibitors, Protein Phosphatase 2, Proto-Oncogene Proteins c-akt, Reactive Oxygen Species, Sodium Selenite

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          Abstract

          We revealed in our previous research that sodium selenite induced obvious apoptosis of human leukemia NB4 cells, with reactive oxygen species (ROS), mitochondrial apoptosis pathway, and endoplasmic reticulum stress (ER stress) involved. In the present study, we revealed protein kinase Ca (PKCalpha) was dramatically downregulated in selenite-induced apoptosis, which was mediated by ROS. Besides, we confirmed PKCalpha played an antiapoptotic role through its effects on ERK1/2 and Akt, while its downregulation was attributed to caspase-3 and PP2Ac under the regulation of ROS. In summary, we speculated that in apoptosis of NB4 cells induced by selenite, PKCalpha functioned to counteract apoptosis, thus its downregulation seemed a mechanism aggravating apoptosis.

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