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首页> 外文期刊>Journal of Cellular Physiology >In vitro and in vivo tumor growth inhibition by a p16-mimicking peptide in p16INK4A-defective, pRb-positive human melanoma cells.
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In vitro and in vivo tumor growth inhibition by a p16-mimicking peptide in p16INK4A-defective, pRb-positive human melanoma cells.

机译：在体外和体内肿瘤生长抑制在p16INK4A-defective p16-mimicking肽,pRb-positive人类黑色素瘤细胞。

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摘要

The cell cycle regulatory pathway responsible for the control of the late-G1 checkpoint is found recurrently altered in human malignant melanoma, often due to lack of functional p16 or pRb (pRb-1) proteins. Here we examined the ability of p16-derived peptides to mimic p16 function in two exemplary human melanoma cell lines: the p16-defective, pRb-positive A375M cells and p16-positive, pRb-defective A2058 cells. The synthetic p16-mimicking peptides strongly induced apoptosis in p16-, pRb+ A375M cells in vitro, while they had significantly less activity on p16+, pRb- A2058 cells. The most active p16-mimicking peptide, p16-AP9, also potently inhibited in vivo growth of the A375M melanoma. Treated tumors showed a threefold smaller volume (P < 0.025) and a significant reduction of the mitotic index and of PCNA expression. Growth of A2058 cells in vivo was not affected by treatment with the p16-mimicking peptide. Our results demonstrate that p16-mimicking peptides can induce apoptosis in vitro and that can inhibit tumor growth in vivo in p16-defective, pRb-expressing human melanoma cells, suggesting that p16-mimicking peptides can represent a promising tool for targeted therapy in selected cancer phenotypes.
机译：细胞周期调控通路负责late-G1检查点的控制地改变了人类恶性黑色素瘤,往往由于缺乏功能性p16或复审委员会(pRb-1)的蛋白质。p16-derived多肽模拟p16在两个函数典型的人类黑色素瘤细胞系:p16-defective, pRb-positive A375M细胞p16-positive, pRb-defective A2058细胞。合成p16-mimicking肽强烈诱导细胞凋亡在p16,复审委员会+ A375M细胞在体外,虽然他们大大减少活动p16 +,复审委员会——A2058细胞。p16-AP9 p16-mimicking肽也有说服力地抑制体内A375M黑色素瘤的生长。治疗肿瘤显示三倍体积较小(P < 0.025),显著降低细胞有丝分裂指数和PCNA的表达。A2058细胞体内没有受到治疗p16-mimicking肽。证明p16-mimicking肽体外诱导细胞凋亡和抑制在p16-defective体内肿瘤的生长,pRb-expressing人类黑色素瘤细胞,这表明p16-mimicking肽可以代表有前途的工具,在选择靶向治疗癌症表型。

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