Carcinogenesis, Vol 18, 1541-1547, Copyright © 1997 by Oxford University Press
R Sinha and D Medina
Methylselenocysteine (MSC), an organic selenium compound has significant
anticarcinogenic activity against mammary tumorigenesis. Previous
experiments have demonstrated that MSC and inorganic selenite inhibit
mammary cell (TM6 cell line) growth through different pathways. The present
investigation demonstrated that MSC arrested cells in S phase during the
TM6 cell cycle, which was followed by cells entering apoptosis at 48 h.
Methylselenocysteine specifically affected the cdk2 kinase activity of the
TM6 cells (54% reduction) at 16 h after release from growth arrest. The
cdk4 kinase activity did not change during the cell cycle, confirming that
cells had passed the G1 checkpoint and had entered S phase. The amount of
cyclin E associated with cdk2 was increased by MSC by the 12 h time point,
thereby facilitating entry of cells into S phase. Afterwards, cyclin E and
cyclin A associated with cdk2 did not change for the remainder of the cell
cycle. The data demonstrate that inhibition of mammary cell growth by MSC
is mediated by alterations in progression of cells through S phase. The
decrease in cdk2 kinase activity is coincident with prolonged arrest in S
phase. One consequence of prolonged arrest may be apoptosis.
ARTICLES
Inhibition of cdk2 kinase activity by methylselenocysteine in synchronized mouse mammary epithelial tumor cells
Cell Biology, Baylor College of Medicine, Houston, TX 77030, USA.
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