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首页> 外文期刊>Life sciences >The p33ING1b tumor suppressor cooperates with p53 to induce apoptosis in response to etoposide in human osteosarcoma cells.
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The p33ING1b tumor suppressor cooperates with p53 to induce apoptosis in response to etoposide in human osteosarcoma cells.

机译：p33ING1b肿瘤抑制因子与p53协同作用，诱导人骨肉瘤细胞中对依托泊苷的凋亡。

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摘要

p33ING1b induces cell cycle arrest and stimulates DNA repair, apoptosis and chemosensitivity. The magnitude of some p33ING1b effects may be due to activation of the tumor suppressor p53. To investigate if the p33ING1b protein affected chemosensitivity of osteosarcoma cells, we overexpressed p33ING1b in p53+/+ U2OS cells or in p53-mutant MG63 cells, and then assessed for growth arrest and apoptosis after treatment with etoposide. p33ING1b increased etoposide-induced growth inhibition and apoptosis to a much greater degree in p53+/+ U2OS cells than in p53-mutant MG63 cells. Moreover, ectopic expression of p33ING1b markedly upregulated p53, p21WAF1 and bax protein levels and activated caspase-3 protein kinase in etoposide-treated U2OS cells. Together, our data indicate that p33ING1b prominently enhances etoposide-induced apoptosis through p53-dependent pathways in human osteosarcoma cells. p33ING1b may be an important marker and/or therapeutic target in the prevention and treatment of metastatic osteosarcoma.
机译：p33ING1b诱导细胞周期停滞并刺激DNA修复，凋亡和化学敏感性。一些p33ING1b效应的强度可能是由于肿瘤抑制因子p53的激活所致。为了研究p33ING1b蛋白是否影响骨肉瘤细胞的化学敏感性，我们在p53 + / + U2OS细胞或p53突变的MG63细胞中过表达p33ING1b，然后评估依托泊苷治疗后的生长停滞和凋亡。与p53突变的MG63细胞相比，p33ING1b在p53 + / + U2OS细胞中增加了依托泊苷诱导的生长抑制和凋亡的作用。此外，在依托泊苷处理的U2OS细胞中，p33ING1b的异位表达显着上调了p53，p21WAF1和bax蛋白水平以及活化的caspase-3蛋白激酶。在一起，我们的数据表明p33ING1b通过人类骨肉瘤细胞中p53依赖性途径显着增强依托泊苷诱导的凋亡。 p33ING1b可能是预防和治疗转移性骨肉瘤的重要标志物和/或治疗靶标。

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