Affiliations: Department of Molecular and Cellular Biology, Baylor
College of Medicine, Houston, TX 77030, USA | Department of Nutritional Sciences, University of
Wisconsin, Madison, WI 53706, USA
Note: [] PhD, 161E, Molecular and Cellular Biology, Baylor College of
Medicine, One Baylor Plaza, Houston, TX 77030, USA. Tel.: +1 713 798 8561; Fax:
+1 713 790 0545; E-mail: rsinha@bcm.tmc.edu
Abstract: Se-methylselenocysteine (MSC) inhibits mouse mammary epithelial
tumor cell (TM6) growth. When synchronized TM6 cells were exposed to 50
μM MSC, either for 30 minutes or continuous, the 116 kDa
poly(ADP-ribose)polymerase (PARP) was cleaved to an 85 kDa fragment indicative
of cells undergoing apoptosis. The earliest cleaved PARP appears at 24 hr time
point followed by elevated levels of 85~kDa fragment at 34 hr and 48 hr time
points when the cells were exposed to continuous treatment with MSC. Results
also showed that MSC increased caspase-3 activity at 24 hr time point. In
addition, continuous treatment with MSC induced DNA fragmentation at 34 hr and
48 hr time points with caspase-3 gene expression moderately increased at 16hr
and 24 hr time points. Caspase-6 and -8 were also involved in the MSC-induced
apoptosis but to a lesser extent. These results suggest that MSC mediates
cleavage of PARP and apoptosis by activating one or more caspases in
synchronized TM6 cells and the events are dependent on the duration of
treatment.
