Posttranscriptional regulation of PTEN dosage by noncoding RNAs.

Posttranscriptional regulation of PTEN dosage by noncoding RNAs.
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DOI:
10.1126/scisignal.3146pe39
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发表时间:
2010-11-02
期刊:
影响因子:
7.3
通讯作者:
He L
He L
中科院分区:
生物学1区
文献类型:
--
作者:
He L

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抑癌基因失活的经典“双击”模型最初是通过对癌症发病率的数学建模建立的,它表明肿瘤的发生需要抑癌基因功能的完全丧失。虽然这在某些肿瘤类型中是正确的,但肿瘤抑制因子解除调控的确切性质取决于组织类型、癌症发展阶段、共存分子病变的性质和环境因素。新出现的证据表明PTEN剂量在肿瘤发展过程中的功能重要性。PTEN剂量的关键调控因子是一些非编码rna,包括microRNAs (miRNAs)和假基因,它们在转录后水平调控PTEN的表达。最近的研究揭示了这些靶向pten的非编码rna在肿瘤发展过程中的功能重要性,并为探索关键癌基因和肿瘤抑制因子剂量依赖性作用的分子机制提供了范例。
The classic “two-hit” model of tumor suppressor inactivation, originally established by mathematical modeling of cancer incidence, implies that tumorigenesis requires complete loss of function of tumor suppressor genes. While this is true in some tumor types, the exact nature of tumor suppressor deregulation varies depending on tissue type, stage of cancer development, nature of co-exisiting molecular lesions, and environmental factors. Emerging evidence has indicated the functional importance of PTEN dosage during tumor development. Among the key regulators of PTEN dosage are a number of non-coding RNAs, including microRNAs (miRNAs) and pseudogenes, which regulate PTEN expression at the post-transcriptional level. Recent studies have revealed the functional importance of these PTEN-targeting non-coding RNAs during tumor development, and have provided a paradigm to explore the molecular mechanisms underlying the dosage-dependent effects of key oncogenes and tumor suppressors.
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