Compelling evidences highlight the critical role of the tumor microenvironment as mediator of tumor progression and immunosuppression in several types of cancer. The reciprocal interplay between neoplastic and non-tumoral host cells is mediated by direct cell-to-cell contact, soluble factors and exosomes that result in differential gene expression patterns that are driven by epigenetic mechanisms. In this regard, extensive literature has described the abnormalities in the DNA methylation status and histone modification profiles in tumor cells. However, little is known about the mechanisms of epigenetic dysregulation that participate as a consequence of the intricate crosstalk among the cells within the tumor niche. This review summarizes the current knowledge on epigenetic changes that result from the interactions between myeloid, stromal and cancer cells in the tumor microenvironment and its functional impact in both tumorigenesis and tumor progression. We also discuss potential niche-specific epigenetic biomarkers to improve the prognosis and clinical treatment of cancer patients.

令人信服的证据凸显了肿瘤微环境在几种类型的癌症中作为肿瘤进展和免疫抑制的介质的关键作用。肿瘤和非肿瘤宿主细胞之间的相互相互作用是由直接的细胞间接触，可溶性因子和外来体介导的，它们导致由表观遗传机制驱动的差异基因表达模式。在这方面，大量文献描述了肿瘤细胞中DNA甲基化状态和组蛋白修饰谱的异常。然而，关于表位遗传失调的机制知之甚少，而表观遗传失调是由于肿瘤位内细胞之间复杂的串扰而参与的。这篇评论总结了有关髓系之间相互作用产生的表观遗传学变化的最新知识，肿瘤微环境中的基质细胞和癌细胞及其在肿瘤发生和肿瘤进展中的功能影响。我们还讨论了潜在的利基特异性表观遗传标记，以改善癌症患者的预后和临床治疗。