国家重点基础研究资助项目(G1999053901).
This work was supported by a grant from The National Basic Research Program of China (G1999053901).
ARF(alternative reading frame)作为INK4a/ARF的β转录产物,能够稳定p53, 诱导细胞周期阻断或凋亡.利用高表达p14ARF的人黑色素瘤细胞模型,探讨了ARF抑制细胞增殖的分子作用机理.研究发现p14ARF高表达能将细胞周期阻断在G1和G2期, p53, p21cip1和p27kip1蛋白水平明显增强, 而p-ERK1/2,CyclinD1和CyclinE蛋白水平下降, 明显抑制细胞生长. 提示p14ARF能通过ERK(extracellular signal-regulated kinase)信号通路相互协调作用抑制A375细胞增殖.
ARF can induce cell cycle arrest or apoptosis. By using the A375 cell overexpressing p14ARF as a model, the molecular machanism of cell cycle arrest by ARF was studied. It was indicated that overexpressing p14ARF resulted in G1-phase and G2-phase arrest. In the A375 cells overexpressing p14ARF, the level of p53, p21cip1 and p27kip1 was upregulated, but the protein lever of p-ERK1/2, Cyclin D1 and Cyclin E was inhibited. The results indicated that p14ARF induced the cell cycle arrest of A375 not only in a p53-dependent way, but also in coopration with the ERK signal transduction pathway.
彭丽霞,张伟,柳惠图,何大澄,高萍.p14ARF对人黑色素瘤细胞增殖的影响及其作用机理的初探[J].生物化学与生物物理进展,2004,31(2):177-180
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