Accessibility of DNA elements and the orchestration of spatiotemporal chromatin-chromatin interactions are critical mechanisms in the regulation of gene transcription. Thus, in an ever-changing milieu, cells mount an adaptive response to environmental stimuli by modulating gene expression that is orchestrated by coordinated changes in chromatin architecture. Correspondingly, agents that alter chromatin structure directly impact transcriptional programs in cells. Heavy metals, including hexavalent chromium (Cr(VI)), are of special interest because of their ability to interact directly with cellular protein, DNA and other macromolecules, resulting in general damage or altered function. In this review we highlight the chromium-mediated mechanisms that promote disruption of chromatin architecture and how these processes are integral to its carcinogenic properties. Emerging evidence shows that Cr(VI) targets nucleosomal architecture in euchromatin, particularly in genomic locations flanking binding sites of the essential transcription factors CTCF and AP1. Ultimately, these changes contribute to an altered chromatin state in critical gene regulatory regions, which disrupts gene transcription in functionally relevant biological processes.

DNA 元素的可及性和时空染色质-染色质相互作用的协调是基因转录调控的关键机制。因此，在不断变化的环境中，细胞通过调节由染色质结构的协调变化协调的基因表达，对环境刺激产生适应性反应。相应地，改变染色质结构的试剂直接影响细胞中的转录程序。包括六价铬 (Cr(VI)) 在内的重金属特别受关注，因为它们能够直接与细胞蛋白质、DNA 和其他大分子相互作用，导致一般损伤或功能改变。在这篇综述中，我们强调了铬介导的促进染色质结构破坏的机制，以及这些过程如何成为其致癌特性的组成部分。新出现的证据表明，Cr(VI) 靶向常染色质中的核小体结构，特别是在基本转录因子 CTCF 和 AP1 结合位点侧翼的基因组位置。最终，这些变化会导致关键基因调控区域的染色质状态发生改变，从而破坏功能相关生物过程中的基因转录。