背景：长非编码RNA（lncRNA）作为通过不同机制调节多种生物过程的新兴调节剂，已被证明在生物学中越来越重要。肿瘤样本的全基因组关联研究已经确定了多种 lncRNA 作为各种癌症的癌基因或肿瘤抑制基因。近年来，lncRNA 的重要性，尤其是在子宫内膜样癌 (EEC) 中的重要性，已得到越来越多的了解。据报道，lncRNA Forkhead box P4 反义 RNA 1 (FOXP4-AS1) 在多种类型的癌症中发挥作用；然而，FOXP4-AS1在EEC中的主要生物学功能和相关的潜在分子机制尚未完全阐明。材料和方法：本研究旨在探讨RNA FOXP4-AS1如何参与子宫内膜样癌组织的发生和进展。为了实现这一目标，在本研究中，我们研究了从医院接受手术的患者收集的子宫内膜样癌组织和与其相匹配的邻近正常子宫内膜组织中FOXP4-AS1的表达水平，并进行了一系列分子生物学检测来研究FOXP4-AS1在子宫内膜样癌组织中的表达水平。 FOXP4-AS1对细胞增殖、细胞迁移、细胞侵袭等的影响。结果：与相应对照相比，在子宫内膜样癌样本和细胞系中发现 FOXP4-AS1 浓度增加，并且发现该 lncRNA 与子宫内膜癌患者的晚期 FIFAO 分期呈正相关。此外，敲低内源性 FOXP4-AS1 会导致子宫内膜样癌细胞中集落形成数量显着减少，并显着抑制细胞增殖、细胞迁移和细胞侵袭。此外，在子宫内膜样癌组织细胞中低表达并受FOXP4-AS1负调节的双特异性磷酸酶5（DUSP5）被确定为FOXP4-AS1的下游靶分子。随后，机制实验证实，通过与zeste同源物2的增强子（EZH2；多梳抑制复合物2 [PRC2]的催化亚基之一）结合，FOXP4-AS1可以表观遗传地抑制DUSP5的表达。最后，通过挽救试验证实了 FOXP4-AS1/EZH2/DUSP5 轴在子宫内膜样癌中的致癌功能。结论：本研究的结果强调了FOXP4-AS1如何在子宫内膜样癌中发挥致癌作用，靶向FOXP4-AS1及其通路可能为子宫内膜样癌患者提供新的生物标志物。

Background: Long noncoding RNAs (lncRNAs), as emerging regulators of a wide variety of biological processes via diverse mechanisms, have been demonstrated to be of increasing importance in biology. Genome-wide association studies of tumor samples have identified several lncRNAs as either oncogenes or tumor suppressors in various types of cancers. In recent years, the importance of lncRNAs, especially in endometrioid cancer (EEC), has become increasingly well understood. The lncRNA Forkhead box P4 antisense RNA 1 (FOXP4-AS1) has been reported to fulfill roles in several types of cancers; however, the main biological function and associated underlying molecular mechanism of FOXP4-AS1 in EEC have yet to be fully elucidated. Materials and Methods: The present study therefore aimed to investigate how RNA FOXP4-AS1 may participate in the development and progression of endometrioid carcinoma tissues. To meet this aim, in the present study, the expression level of FOXP4-AS1 was investigated in endometrioid carcinoma tissues and matching nearby normal endometrial tissues collected from patients receiving surgery at the hospital, and a series of molecular biological assays were performed to investigate the effect of FOXP4-AS1 on cell proliferation, cell migration, and cell invasion, and so on. Results: An increased concentration of FOXP4-AS1 was identified in endometrioid carcinoma samples and cell lines compared with the corresponding controls, and this lncRNA was found to be positively correlated with advanced FIGO stages in patients with endometrial cancer. Furthermore, knocking down endogenous FOXP4-AS1 led to a significant reduction in the colony formation number and a significant inhibition of cell proliferation, cell migration, and cell invasion in endometrioid carcinoma cells. Moreover, dual-specificity phosphatase 5 (DUSP5), which is lowly expressed in endometrioid carcinoma tissues cells and negatively modulated by FOXP4-AS1, was identified as the downstream target molecule of FOXP4-AS1. Subsequently, the mechanistic experiments confirmed that, through binding to enhancer of zeste homolog 2 (EZH2; one of the catalytic subunits of polycomb repressive complex 2 [PRC2]), FOXP4-AS1 could epigenetically suppress the expression of DUSP5. Finally, the oncogenic function of the FOXP4-AS1/EZH2/DUSP5 axis in endometrioid carcinoma was confirmed via rescue assays. Conclusions: The findings of the present study have highlighted how FOXP4-AS1 fulfills an oncogenic role in endometrioid carcinoma, and targeting FOXP4-AS1 and its pathway may provide new biomarkers for patients with endometrioid carcinoma.