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Co-regulation of senescence-associated genes by oncogenic homeobox proteins and polycomb repressive complexes

机译：致癌同源异形盒蛋白和多梳抑制复合物对衰老相关基因的共同调控

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摘要

Cellular senescence is a stable cell cycle arrest that can be induced by stresses such as telomere shortening, oncogene activation or DNA damage. Senescence is a potent anticancer barrier that needs to be circumvented during tumorigenesis. The cell cycle regulator p16INK4a is a key effector upregulated during senescence. Polycomb repressive complexes (PRCs) play a crucial role in silencing the INK4/ARF locus, which encodes for p16 INK4a, but the mechanisms by which PRCs are recruited to this locus as well as to other targets remain poorly understood. Recently we discovered the ability of the homeobox proteins HLX1 (H2.0-like homeobox 1) and HOXA9 (Homeobox A9) to bypass senescence. We showed that HLX1 and HOXA9 recruit PRCs to repress INK4a, which constitutes a key mechanism explaining their effects on senescence. Here we provide evidence for the regulation of additional senescence-associated PRC target genes by HLX1 and HOXA9. As both HLX1 and HOXA9 are oncogenes implicated in leukemogenesis, we discuss the implications that the collaboration between Homeobox proteins and PRCs has for senescence and cancer.
机译：细胞衰老是一种稳定的细胞周期停滞，可通过诸如端粒缩短，癌基因激活或DNA损伤等压力诱导。衰老是一种有效的抗癌屏障，需要在肿瘤发生过程中加以规避。细胞周期调节因子p16INK4a是衰老过程中上调的关键效应子。聚梳抑制复合物（PRC）在沉默INK4 / ARF基因座中起关键作用，INK4 / ARF基因座编码p16 INK4a，但是对PRCs募集到该基因座以及其他靶标的机制仍知之甚少。最近，我们发现了同源盒蛋白HLX1（类似于H2.0的同源盒1）和HOXA9（同源盒A9）绕过衰老的能力。我们显示HLX1和HOXA9募集PRC来抑制INK4a，这构成了解释其对衰老影响的关键机制。在这里，我们为HLX1和HOXA9调控其他与衰老相关的PRC靶基因提供了证据。由于HLX1和HOXA9都是与白血病发生有关的癌基因，因此我们讨论Homeobox蛋白与PRCs之间的协作对衰老和癌症的影响。

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