摘要
Tumor suppressor ARF can induce cell cycle arrest or apoptosis by activating p53. In order to explore the molecular mechanism of the induction of apoptosis by p14ARF, a human melanoma cell model overexpressing p14ARF was constructed. Present study indicated that in the cells overex-pressing p14ARF, p53 was accumulated in nucleus while it dispersed in cytosol in the control cells. Irradiated with g-ray, overexpressing p14ARF promoted the apoptosis of A375 cells, triggered Smac release from mitochondria to cytosol, and increased the expression of p53, Bax, Caspase-3, Caspase-9, p21cip1 and p27kip1. However, the protein level of Bcl-2 and phospho-ERK was down-regulated. These results suggested a possible mechanism of p14ARF in promotion of apoptosis.
Tumor suppressor ARF can induce cell cycle arrest or apoptosis by activating p53. In order to explore the molecular mechanism of the induction of apoptosis by p14ARF, a human melanoma cell model overexpressing p14ARF was constructed. Present study indicated that in the cells overex-pressing p14ARF, p53 was accumulated in nucleus while it dispersed in cytosol in the control cells. Irradiated with g-ray, overexpressing p14ARF promoted the apoptosis of A375 cells, triggered Smac release from mitochondria to cytosol, and increased the expression of p53, Bax, Caspase-3, Caspase-9, p21cip1 and p27kip1. However, the protein level of Bcl-2 and phospho-ERK was down-regulated. These results suggested a possible mechanism of p14ARF in promotion of apoptosis.
