Inhibition of mitotic cyclin B and cdc2 kinase activity by selenomethionine in synchronized colon cancer cells

M. Chigbrow, Mark A Nelson

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

Selenomethionine (SeMet), an organic selenium compound, has been demonstrated to have significant chemopreventive activity. However, the mechanism of action of SeMet has yet to be identified. Previously, our laboratory found that treatment of cells with SeMet induced apoptosis and altered the cell cycle. These observations have led to further analysis of the cell cycle effects of SeMet in colon cancer cells. Synchronized HCT 116 colon cancer cells treated with 100 μM SeMet for 66 h were found to have a transient delay in G2/M phase of the cell cycle at 18 and 24 h after treatment. With this was observed an inhibition of cell growth. Coincidentally with this delay was a decrease in mitotic cyclin B RNA expression at 18 h After treatment. In addition, the cdc2 kinase activity of HCT 116 cells was decreased at 18 h. Morphological studies indicate an increase in the number of treated cells (45%) undergoing apoptosis at 66 h compared to control cells (27%). These studies demonstrate that modulation of mitotic cyclin expression and cdc2 kinase activity play a role in the ability of SeMet to inhibit tumor cell growth. A consequence of this prolonged arrest is apoptosis.

Original languageEnglish (US)
Pages (from-to)43-50
Number of pages8
JournalAnti-Cancer Drugs
Volume12
Issue number1
DOIs
StatePublished - 2001

Fingerprint

Selenomethionine
Cyclin B
Colonic Neoplasms
Phosphotransferases
Cell Cycle
Apoptosis
Selenium Compounds
HCT116 Cells
Cyclins
G2 Phase
Growth
Cell Division
Cell Count
RNA
Neoplasms

Keywords

  • CDC2
  • Colon cancer
  • Cyclin B
  • Selenomethionine

ASJC Scopus subject areas

  • Pharmacology
  • Cancer Research
  • Oncology

Cite this

Inhibition of mitotic cyclin B and cdc2 kinase activity by selenomethionine in synchronized colon cancer cells. / Chigbrow, M.; Nelson, Mark A.

In: Anti-Cancer Drugs, Vol. 12, No. 1, 2001, p. 43-50.

Research output: Contribution to journalArticle

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