Sodium selenite increases the activity of the tumor suppressor protein, PTEN, in DU-145 prostate cancer cells

Nutr Cancer. 2009;61(3):322-31. doi: 10.1080/01635580802521338.

Abstract

Epidemiological and clinical data suggest that selenium may prevent prostate cancer; however, the cellular effects of selenium in malignant prostate cells are not well understood. We previously reported that the activity of the tumor suppressor PTEN is modulated by thioredoxin (Trx) in a RedOx-dependent manner. In this study, we demonstrated that the activity of Trx reductase (TR) is increased by sevenfold in the human prostate cancer cell line, DU-145, after 5 days of sodium selenite (Se) treatment. The treatment of DU-145 cells with increasing concentrations of Se induced an increase in PTEN lipid phosphatase activity by twofold, which correlated with a decrease in phospho-ser(473)-Akt, and an increase in phospho-Ser(370)-PTEN levels. Se also increased casein kinase-2 (CK2) activity; and the use of apigenin, an inhibitor of CK2, revealed that the regulation of the tumor suppressor PTEN by Se may be achieved via both the Trx-TR system and the RedOx control of the kinase involved in the regulation of PTEN activity.

MeSH terms

  • Casein Kinase II / physiology
  • Cell Line, Tumor
  • Glutathione / metabolism
  • Humans
  • Male
  • PTEN Phosphohydrolase / metabolism*
  • Phosphorylation
  • Prostatic Neoplasms / enzymology*
  • Prostatic Neoplasms / pathology
  • Proto-Oncogene Proteins c-akt / metabolism
  • Sodium Selenite / pharmacology*
  • Thioredoxin-Disulfide Reductase / metabolism
  • Thioredoxins / metabolism
  • Tumor Suppressor Proteins / analysis*

Substances

  • Tumor Suppressor Proteins
  • Thioredoxins
  • Thioredoxin-Disulfide Reductase
  • Casein Kinase II
  • Proto-Oncogene Proteins c-akt
  • PTEN Phosphohydrolase
  • PTEN protein, human
  • Glutathione
  • Sodium Selenite