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首页> 外文期刊>British Journal of Cancer >The expression of p53-induced protein with death domain (Pidd) and apoptosis in oral squamous cell carcinoma
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The expression of p53-induced protein with death domain (Pidd) and apoptosis in oral squamous cell carcinoma

机译:口腔鳞状细胞癌中p53诱导的具有死亡结构域(Pidd)和凋亡的蛋白的表达

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The Pidd (p53-induced protein with death domain) gene was shown to be induced by the tumour suppressor p53 and to mediate p53-dependent apoptosis in mouse and human cells, through interactions with components of both the mitochondrial and the death receptor signalling pathways. To study the role of Pidd in clinical tumours, we measured its expression by quantitative reverse transcription-PCR in microdissected oral squamous cell carcinomas (OSCC) with and without p53 mutation. Tumour cell apoptosis was assessed by in situ terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling. Tumour proliferation was assessed by immunohistochemical staining for the Ki-67 antigen. We found a wide range of Pidd expression among OSCC. Statistical analysis revealed an association between Pidd expression and apoptotic index (Mann–Whitney test, PPidd in apoptosis in this tumour type. Furthermore, we showed a positive correlation between apoptotic index and proliferative index that has not been previously described for OSCC. There was no correlation between Pidd expression and the p53 mutation status of these tumours, suggesting that Pidd expression may be regulated by p53-independent mechanisms. Further characterisation of these molecular defects in the control of proliferation and apoptosis should help in developing treatments that target OSCC according to their biological properties.
机译:通过与线粒体和死亡受体信号传导途径的相互作用,Pidd(p53诱导的具有死亡结构域的蛋白)基因已被肿瘤抑制p53诱导,并介导小鼠和人类细胞中p53依赖性凋亡。为了研究Pidd在临床肿瘤中的作用,我们通过定量逆转录PCR检测了有或无p53突变的口腔鳞状细胞癌(OSCC)中Pidd的表达。通过原位末端脱氧核苷酸转移酶介导的dUTP缺口末端标记评估肿瘤细胞凋亡。通过免疫组织化学Ki-67抗原评估肿瘤增殖。我们在OSCC中发现了各种各样的Pidd表达。统计分析显示,Pidd表达与细胞凋亡指数之间存在相关性(Mann-Whitney检验,PPid参与该类型肿瘤的凋亡。此外,我们发现凋亡指数与增殖指数之间呈正相关,这在OSCC中尚无记载。 Pidd表达与这些肿瘤的p53突变状态之间的相关性,提示Pidd表达可能受p53独立机制的调控,这些分子缺陷在增殖和凋亡控制中的进一步表征应有助于开发针对OSCC的靶向治疗方法生物学特性。

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