Accumulating evidence has suggests that women with advanced endometriosis exhibit alterations in the expression of genes in the endometrium compared to healthy controls. Furthermore, replication stress is a characteristic feature of cancer cells, which results from sustained proliferative signaling induced by either the activation of oncogenes or the loss of tumor suppressors. In the present study, we propose that DNA replication ATP-dependent helicase/nuclease 2 (DNA2) might be upregulated in endometriosis. Immunohistochemical staining results confirmed the hypothesis that DNA2 is overexpressed in the eutopic/ectopic endometrium compared to that in a control endometrium from a healthy donor. Subsequently, ectopic endometrium-derived endometrial mesenchymal stem cells (EMSCs) showed the highest level of DNA2 and checkpoint kinase 1 (CHK1), as well as the strongest proliferation and migration capabilities, followed by eutopic endometrium-derived EMSCs, and then control EMSCs. To further analyze the function of DNA2, we knocked-down DNA2 expression in KLE cells. As expected, proliferation and migration declined when cells were transfected with DNA2 small interfering RNA. Taken together, our study demonstrated the overexpression of DNA2 in human endometriosis, which might be responsible for the upregulated cell proliferation and migration. This study provides insights into the mechanisms underlying human endometriosis.

越来越多的证据表明，与健康对照组相比，患有晚期子宫内膜异位症的女性在子宫内膜中表现出基因表达的改变。此外，复制应激是癌细胞的一个特征，它是由癌基因激活或肿瘤抑制因子丧失诱导的持续增殖信号传导引起的。在本研究中，我们提出 DNA 复制 ATP 依赖性解旋酶/核酸酶 2 (DNA2) 可能在子宫内膜异位症中上调。免疫组织化学染色结果证实了与健康供体的对照子宫内膜相比，DNA2 在在位/异位子宫内膜中过度表达的假设。随后，异位子宫内膜来源的子宫内膜间充质干细胞（EMSCs）显示出最高水平的DNA2和检查点激酶1（CHK1），以及最强的增殖和迁移能力，其次是在位子宫内膜来源的 EMSCs，然后是控制 EMSCs。为了进一步分析 DNA2 的功能，我们敲低了 KLE 细胞中的 DNA2 表达。正如预期的那样，当细胞用 DNA2 小干扰 RNA 转染时，增殖和迁移下降。总之，我们的研究证明了 DNA2 在人类子宫内膜异位症中的过表达，这可能是细胞增殖和迁移上调的原因。这项研究提供了对人类子宫内膜异位症潜在机制的见解。当用 DNA2 小干扰 RNA 转染细胞时，增殖和迁移能力下降。总之，我们的研究证明了 DNA2 在人类子宫内膜异位症中的过表达，这可能是细胞增殖和迁移上调的原因。这项研究提供了对人类子宫内膜异位症潜在机制的见解。当用 DNA2 小干扰 RNA 转染细胞时，增殖和迁移能力下降。总之，我们的研究证明了 DNA2 在人类子宫内膜异位症中的过表达，这可能是细胞增殖和迁移上调的原因。这项研究提供了对人类子宫内膜异位症潜在机制的见解。