Biochemical effects of type i interferons on prostate cancer cell cycle.

Conference Paper

Prostate cancer is a serious health risk for men that has a marked agerelated increase in incidence. Tumors of the prostate, as with other types of cancer, have been found to be related to the loss of cell cycle control resulting in increased growth of cells. Recently, a gene coding for a metastatic suppressor, KAI1, has been associated with prostate cancer. For this reason, we have looked at the biochemistry behind the regulation of the prostate cancer cell cycle by type I Interferon (IFN). Using the androgen independent MatLyLu subline of the Dunning rat prostate carcinoma, we carried out cell cycle analysis of the antiproliferative effects of rat IFN o/p on these cells. The type I IFNs have both antiviral and anti-proliferative effects on the MatLyLu cells, and analysis by propidium idodide staining shows that rat IFN a/β slows the progression of the cells through the S phase of the cell cycle. Consistent with this data, we have shown that rat IFN a/β treated MatLyLu cells have a decrease in the level of cyclin dependent kinase 2 (cdk2) activity. Interferon regulation of cdk2 activity and cyclins in the cell cycle may be important in the mechanism of the anti-tumor effects of interferons.

Duke Authors

Cited Authors

  • Hobeika, A; Subramaniam, PS; Johnson, HM

Published Date

  • December 1, 1996

Published In

Volume / Issue

  • 10 / 6

International Standard Serial Number (ISSN)

  • 0892-6638

Citation Source

  • Scopus