Cancer Epigenetics and Nanomedicine Laboratory, Nanomaterials and Nanotechnology Research Center (CINN-CSIC), University of Oviedo, Oviedo, Spain.
Institute of Oncology of Asturias (IUOPA), University of Oviedo, Oviedo, Spain.
Mol Biol Evol. 2021 Jul 29;38(8):3415-3435. doi: 10.1093/molbev/msab112.
Aging and cancer are two interrelated processes, with aging being a major risk factor for the development of cancer. Parallel epigenetic alterations have been described for both, although differences, especially within the DNA hypomethylation scenario, have also been recently reported. Although many of these observations arise from the use of mouse models, there is a lack of systematic comparisons of human and mouse epigenetic patterns in the context of disease. However, such comparisons are significant as they allow to establish the extent to which some of the observed similarities or differences arise from pre-existing species-specific epigenetic traits. Here, we have used reduced representation bisulfite sequencing to profile the brain methylomes of young and old, tumoral and nontumoral brain samples from human and mouse. We first characterized the baseline epigenomic patterns of the species and subsequently focused on the DNA methylation alterations associated with cancer and aging. Next, we described the functional genomic and epigenomic context associated with the alterations, and finally, we integrated our data to study interspecies DNA methylation levels at orthologous CpG sites. Globally, we found considerable differences between the characteristics of DNA methylation alterations in cancer and aging in both species. Moreover, we describe robust evidence for the conservation of the specific cancer and aging epigenomic signatures in human and mouse. Our observations point toward the preservation of the functional consequences of these alterations at multiple levels of genomic regulation. Finally, our analyses reveal a role for the genomic context in explaining disease- and species-specific epigenetic traits.
衰老和癌症是两个相互关联的过程,衰老也是癌症发生的一个主要危险因素。尽管已经描述了这两个过程中存在平行的表观遗传改变,但最近也报道了它们之间的差异,尤其是在 DNA 低甲基化方面。尽管这些观察结果中的许多是从使用小鼠模型得出的,但在疾病背景下,人类和小鼠的表观遗传模式之间缺乏系统的比较。然而,这样的比较是重要的,因为它们可以确定一些观察到的相似性或差异性在多大程度上是由于预先存在的物种特异性表观遗传特征所致。在这里,我们使用简化代表性重亚硫酸盐测序来分析来自人类和小鼠的年轻和年老、肿瘤和非肿瘤脑组织样本的大脑甲基组。我们首先描述了物种的基线表观基因组模式,然后重点研究了与癌症和衰老相关的 DNA 甲基化改变。接下来,我们描述了与这些改变相关的功能基因组和表观基因组背景,最后,我们整合了我们的数据来研究在同源 CpG 位点上的种间 DNA 甲基化水平。总体而言,我们在两个物种的癌症和衰老的 DNA 甲基化改变的特征之间发现了相当大的差异。此外,我们描述了在人类和小鼠中,特定的癌症和衰老表观遗传特征的稳健证据。我们的观察结果表明,这些改变在多个基因组调控水平上的功能后果得到了保留。最后,我们的分析揭示了基因组背景在解释疾病和物种特异性表观遗传特征方面的作用。