三阴性乳腺癌（TNBC）是一种高度侵袭性乳腺癌亚型，治疗选择有限。与其他乳腺癌亚型不同，特定疗法的缺乏和远处转移的频率较高导致其侵袭性。我们的目标是找到有助于理解这些癌症传播过程的表观遗传变化。使用 CRISPR/Cas9，我们的实验方法使我们识别并破坏了绝缘体元件 IE8，其活性似乎与细胞侵袭相关。实验在两种成熟的 TNBC 细胞模型 MDA-MB-231 和 MDA-MB-436 中进行。为了深入了解 TNBC 侵袭能力的潜在分子机制，我们在两种细胞模型中生成并表征了高分辨率染色质相互作用 (Hi-C) 和染色质可及性 (ATAC-seq) 图谱，并用基因表达谱 (RNA) 补充了这些数据集。 -seq）在 MDA-MB-231 中，该细胞系在染色质可及性方面表现出更显着的变化。总而言之，我们的数据为了解 TNBC 细胞基因组的空间组织提供了全面的资源，这可能有助于加速发现 TNBC 特异性改变，从而引发这种毁灭性疾病的进展。© 2023。作者。

Triple-negative breast cancer (TNBC) is a highly aggressive breast cancer subtype with limited treatment options. Unlike other breast cancer subtypes, the scarcity of specific therapies and greater frequencies of distant metastases contribute to its aggressiveness. We aimed to find epigenetic changes that aid in the understanding of the dissemination process of these cancers.Using CRISPR/Cas9, our experimental approach led us to identify and disrupt an insulator element, IE8, whose activity seemed relevant for cell invasion. The experiments were performed in two well-established TNBC cellular models, the MDA-MB-231 and the MDA-MB-436. To gain insights into the underlying molecular mechanisms of TNBC invasion ability, we generated and characterized high-resolution chromatin interaction (Hi-C) and chromatin accessibility (ATAC-seq) maps in both cell models and complemented these datasets with gene expression profiling (RNA-seq) in MDA-MB-231, the cell line that showed more significant changes in chromatin accessibility. Altogether, our data provide a comprehensive resource for understanding the spatial organization of the genome in TNBC cells, which may contribute to accelerating the discovery of TNBC-specific alterations triggering advances for this devastating disease.© 2023. The Author(s).