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首页> 外文期刊>Pathobiology: journal of immunopathology, molecular and cellular biology >p16 Gene Transfer Induces Centrosome Amplification and Abnormal Nucleation Associated with Survivin Downregulation in Glioma Cells
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p16 Gene Transfer Induces Centrosome Amplification and Abnormal Nucleation Associated with Survivin Downregulation in Glioma Cells

机译：p16基因转移诱导神经胶质瘤细胞中与survivin下调相关的中心体扩增和异常成核。

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Objective: In human glioma cells, p16 gene transfer induced G1/S arrest, increased radiosensitivity and abnormal nucleation (especially bi- and multinucleation). Survivin suppression caused G2/M arrest, radiosensitization and an increase in aneuploidy accompanied by centrosome amplification. Abnormal nucleation and aneuploidy represent chromosome instability (CIN), and it is well known that centrosome amplification leads to CIN. However, little has been reported that suggests that transferring p16 causes centrosome over-duplication during the G1/S phase. Methods: The p16 gene was transferred into p16-null human glioma cell lines (U251MG and D54MG) using adenovirus with or without irradiation. Centrosome amplification was evaluated by immunofluorescence. We also investigated the DNA replication licensing factor CDT1, its inhibitor geminin and survivin expression as regulators of chromosomal segregation. Results: p16 gene transfer with radiation initiated the greatest degree of centrosome overduplication. CDT1 showed low levels, geminin was unchanged and survivin decreased in Ax-hp16-infected cells with radiation. Those changes of factors affecting DNA licensing or chromosomal segregation might contribute to CIN. Conclusion: p16 transfer caused centrosome amplification even in G1/S phase-arrested cells. This suggests that p16 is involved in abnormal nucleation and radiosensitization in human glioma cells. (C) 2015 S. Karger AG, Basel
机译：目的：在人类神经胶质瘤细胞中，p16基因转移导致G1 / S阻滞，放射敏感性增加和异常成核（尤其是双核和多核）。 Survivin抑制导致G2 / M阻滞，放射增敏和非整倍性增加，并伴随着中心体扩增。异常的成核和非整倍性代表染色体不稳定性（CIN），众所周知，中心体扩增会导致CIN。然而，几乎没有报道表明转移p16会在G1 / S期引起中心体过度复制。方法：使用腺病毒在有或没有辐射的情况下，将p16基因转移到无p16人胶质瘤细胞系（U251MG和D54MG）中。通过免疫荧光评估中心体扩增。我们还研究了DNA复制许可因子CDT1，其抑制剂geminin和survivin表达作为染色体分离的调控因子。结果：p16基因在辐射下的转移引发了最大程度的中心体过度复制。在用放射线感染Ax-hp16的细胞中，CDT1显示出低水平，geminin不变，survivin下降。影响DNA许可或染色体分离的因素的那些变化可能有助于CIN。结论：即使在G1 / S期停滞的细胞中，p16转移也会引起中心体扩增。这表明p16参与人类神经胶质瘤细胞的异常成核和放射增敏作用。 （C）2015 S.Karger AG，巴塞尔

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