TY - JOUR
T1 - ALG-2 knockdown in HeLa cells results in G2/M cell cycle phase accumulation and cell death
AU - Høj, Berit Rahbek
AU - la Cour, Peter Jonas Marstrand
AU - Mollerup, Jens
AU - Berchtold, Martin Werner
N1 - KEYWORDS: Calcium-binding proteins; Apoptosis-linked gene-2 (ALG-2); siRNA; Apoptosis; Cell cycle; Caspase
PY - 2009
Y1 - 2009
N2 - ALG-2 (apoptosis-linked gene-2 encoded protein) has been shown to be upregulated in a variety of human tumors questioning its previously assumed pro-apoptotic function. The aim of the present study was to obtain insights into the role of ALG-2 in human cancer cells. We show that ALG-2 downregulation induces accumulation of HeLa cells in the G2/M cell cycle phase and increases the amount of early apoptotic and dead cells. Caspase inhibition by the pan-caspase inhibitor zVAD-fmk attenuated the increase in the amount of dead cells following ALG-2 downregulation. Thus, our results indicate that ALG-2 has an anti-apoptotic function in HeLa cells by facilitating the passage through checkpoints in the G2/M cell cycle phase.
AB - ALG-2 (apoptosis-linked gene-2 encoded protein) has been shown to be upregulated in a variety of human tumors questioning its previously assumed pro-apoptotic function. The aim of the present study was to obtain insights into the role of ALG-2 in human cancer cells. We show that ALG-2 downregulation induces accumulation of HeLa cells in the G2/M cell cycle phase and increases the amount of early apoptotic and dead cells. Caspase inhibition by the pan-caspase inhibitor zVAD-fmk attenuated the increase in the amount of dead cells following ALG-2 downregulation. Thus, our results indicate that ALG-2 has an anti-apoptotic function in HeLa cells by facilitating the passage through checkpoints in the G2/M cell cycle phase.
U2 - 10.1016/j.bbrc.2008.11.021
DO - 10.1016/j.bbrc.2008.11.021
M3 - Journal article
C2 - 19013425
SN - 0006-291X
VL - 378
SP - 145
EP - 148
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 1
ER -
