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首页> 外文期刊>Cellular & molecular biology letters. >Inhibitor of differentiation 1 (ID1) promotes cell survival and proliferation of prostate epithelial cells.
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Inhibitor of differentiation 1 (ID1) promotes cell survival and proliferation of prostate epithelial cells.

机译：分化抑制剂1（ID1）促进前列腺上皮细胞的存活和增殖。

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摘要

Id1 (inhibitor of differentiation 1) is a member of the bHLH protein family. Consistent with its role in promoting proliferation and inhibiting differentiation, Id1 expression is low or negligible in normal prostate epithelial cells but is high in prostate cancer. Ectopic expression of Id1 in normal prostate epithelial cells could therefore provide a model for understanding early events involved in initiation of prostate cancer. Over-expression of Id1 immortalized but did not transform ventral prostate epithelial cells (Id1-RPE). Immortalization was associated with decreased Cdkn2a, Cdkn1a, androgen receptor and increased Tert expression. Gene expression profiling over successive doublings was used to identify transcriptomic changes involved during immortalization (Tieg, Jun, alpha actin, Klf10, Id2) and in maintaining the immortalized phenotype (Igfbp3, Igfbp5, Mmp2, Tgfb3). Network analysis indicated that Id1 promotes cancer/tumor morphology, cell cycle and epithelial to mesenchymal transition by influencing AP1, tnf, tgfbeta, PdgfBB and estradiol pathways. During immortalization, the expression of majority of differentially expressed genes reduced over progressive doublings suggesting a decline in transcriptional regulatory mechanisms. The associated molecular/gene expression profile of Id1-RPE cells provides an opportunity to understand the molecular pathways associated with prostate epithelial cell survival and proliferation.
机译：Id1（分化抑制剂1）是bHLH蛋白家族的成员。与它在促进增殖和抑制分化中的作用一致，Id1表达在正常前列腺上皮细胞中较低或可忽略不计，但在前列腺癌中较高。因此，正常前列腺上皮细胞中Id1的异位表达可以提供一个模型，以了解参与前列腺癌发病的早期事件。 Id1的过量表达永生，但并未转化腹侧前列腺上皮细胞（Id1-RPE）。永生化与减少Cdkn2a，Cdkn1a，雄激素受体和增加Tert表达有关。连续倍增的基因表达谱用于鉴定永生化​​（Tieg，Jun，α肌动蛋白，Klf10，Id2）和维持永生化表型（Igfbp3，Igfbp5，Mmp2，Tgfb3）涉及的转录组变化。网络分析表明，Id1通过影响AP1，tnf，tgfbeta，PdgfBB和雌二醇途径来促进癌症/肿瘤形态，细胞周期以及上皮向间质的转化。在永生化过程中，大多数差异表达基因的表达比进行性加倍降低，表明转录调控机制下降。 Id1-RPE细胞的相关分子/基因表达谱为了解与前列腺上皮细胞存活和增殖相关的分子途径提供了机会。

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