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特里斯特拉普罗林减弱了myc诱导的淋巴瘤,并废除了恶性状态

Robert J Rounbehler¹, Mohammad Fallahi, Chunying Yang

¹Department of Cancer Biology, The Scripps Research Institute, Scripps Florida, Jupiter, FL 33458, USA.

|August 7, 2012

概括

Myc oncoprotein通过AU结合蛋白 (AUBPs) 调节mRNA周转,从而影响基因表达. 抑制甲 (TTP) 是Myc驱动癌症的关键,TTP作为瘤抑制剂.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
基因法规基因法规

背景情况:

Myccoproteins影响基因转录,但Myc调节的基因中有很大一部分涉及转录后的机制.
mRNA周转是由AU结合蛋白 (AUBPs) 调节的,这些蛋白与转录中的AU丰富元素 (ARE) 相互作用.
了解Myc对AUBPs和ARE含有的 (ARED) 基因的影响对于破译其在瘤发生中的作用至关重要.

研究的目的:

通过AUBPs和ARED基因,研究Myccoproteins如何调节mRNA周转.
为了确定Tristetraprolin (TTP/ZFP36),一个AUBP在Myc驱动的淋巴发育中的作用.
阐明Myc影响TTP表达的机制及其在癌症中的后果.

主要方法:

对癌前和恶性Myc表达B细胞的分析.
评估Myc对TTP和其他ARED基因的直接转录调节.
评估TTP在Myc诱导的淋巴发育和癌症维持中的功能.

主要成果:

在B细胞中,Myc调节了数百个ARED基因和特定的AUBP.
Myc直接抑制了mRNA破坏稳定的AUBP,Tristetraprolin (TTP) 的转录.
TTP抑制是MYC涉及的癌症的标志,其恢复抑制了淋巴发育,表明TTP作为瘤抑制剂.

结论:

Myc利用AUBPs,特别是TTP,来控制参与瘤发生的ARED基因.
Myc对TTP的抑制是B淋巴发育和IL7信号传递中的关键电路,其失调被选择用于恶性瘤.
针对Myc-TTP轴为MYC驱动的癌症提供了潜在的治疗策略.

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