Structural maintenance of chromosomes 4 (SMC4) has an important role in chromosome condensation and segregation, which is involved in regulating multiple tumor development. However, the role of SMC4 in endometrial cancer is uncertain. The expression and prognostic value of SMC4 were predicted by UALCAN, Gene Expression Omnibus (GEO), The Human Protein Atlas and Kaplan Meier plotter tools. SMC4-related genes were analyzed by LinkedOmics, Gene Ontology (GO) annotations, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Forkhead box protein O1 (FoxO1) activity was suppressed by AS1842856 (AS). SMC4, Ki67, B-cell lymphoma-2(Bcl-2), Bcl-2 associated X protein (Bax), FoxO1, phosphorylated FoxO1 (p-FoxO1), and p27 protein levels were detected by Western blotting. Cell proliferation was detected using Cell Counting Kit-8 (CCK-8) and 5-ethynyl-2′-deoxyuridine (EdU) analyses. Cell apoptosis was measured using TUNEL analysis. SMC4 abundance was increased in endometrial cancer, and predicted a worse overall survival. SMC4 knockdown repressed proliferative ability of endometrial cancer cells and promoted cell apoptosis. SMC4 knockdown promoted FoxO1 transactivation by decreasing its phosphorylated level. Addition of AS inhibited FoxO1 activity by increasing the phosphorylated level of FoxO1. The inhibition of FoxO1 activity reversed the effect of SMC4 silencing on cell proliferation and apoptosis. In conclusion, SMC4 silencing restrained cell proliferation and facilitated apoptosis in endometrial cancer via regulating FoxO1 activity.

4号染色体结构维持（SMC4）在染色体凝聚和分离中具有重要作用，参与调控多种肿瘤的发展。然而，SMC4 在子宫内膜癌中的作用尚不确定。SMC4 的表达和预后价值由 UALCAN、基因表达综合 (GEO)、人类蛋白质图谱和 Kaplan Meier 绘图仪工具预测。SMC4 相关基因通过 LinkedOmics、基因本体 (GO) 注释和京都基因和基因组百科全书 (KEGG) 通路富集分析进行分析。Forkhead box 蛋白 O1 (FoxO1) 活性被 AS1842856 (AS) 抑制。通过蛋白质印迹检测 SMC4、Ki67、B 细胞淋巴瘤-2(Bcl-2)、Bcl-2 相关 X 蛋白 (Bax)、FoxO1、磷酸化 FoxO1 (p-FoxO1) 和 p27 蛋白水平。使用细胞计数试剂盒-8 (CCK-8) 和 5-乙炔基-2'-脱氧尿苷 (EdU) 分析检测细胞增殖。使用TUNEL分析测量细胞凋亡。SMC4 丰度在子宫内膜癌中增加，并预测更差的总生存期。SMC4 敲低抑制子宫内膜癌细胞的增殖能力并促进细胞凋亡。SMC4 敲低通过降低其磷酸化水平来促进 FoxO1 反式激活。添加 AS 通过增加 FoxO1 的磷酸化水平来抑制 FoxO1 的活性。FoxO1 活性的抑制逆转了 SMC4 沉默对细胞增殖和凋亡的影响。总之，SMC4沉默通过调节FoxO1活性抑制子宫内膜癌的细胞增殖并促进细胞凋亡。使用TUNEL分析测量细胞凋亡。SMC4 丰度在子宫内膜癌中增加，并预测更差的总生存期。SMC4 敲低抑制子宫内膜癌细胞的增殖能力并促进细胞凋亡。SMC4 敲低通过降低其磷酸化水平来促进 FoxO1 反式激活。添加 AS 通过增加 FoxO1 的磷酸化水平来抑制 FoxO1 的活性。FoxO1 活性的抑制逆转了 SMC4 沉默对细胞增殖和凋亡的影响。总之，SMC4沉默通过调节FoxO1活性抑制子宫内膜癌的细胞增殖并促进细胞凋亡。使用TUNEL分析测量细胞凋亡。SMC4 丰度在子宫内膜癌中增加，并预测更差的总生存期。SMC4 敲低抑制子宫内膜癌细胞的增殖能力并促进细胞凋亡。SMC4 敲低通过降低其磷酸化水平来促进 FoxO1 反式激活。添加 AS 通过增加 FoxO1 的磷酸化水平来抑制 FoxO1 的活性。FoxO1 活性的抑制逆转了 SMC4 沉默对细胞增殖和凋亡的影响。总之，SMC4沉默通过调节FoxO1活性抑制子宫内膜癌的细胞增殖并促进细胞凋亡。SMC4 敲低抑制子宫内膜癌细胞的增殖能力并促进细胞凋亡。SMC4 敲低通过降低其磷酸化水平来促进 FoxO1 反式激活。添加 AS 通过增加 FoxO1 的磷酸化水平来抑制 FoxO1 的活性。FoxO1 活性的抑制逆转了 SMC4 沉默对细胞增殖和凋亡的影响。总之，SMC4沉默通过调节FoxO1活性抑制子宫内膜癌的细胞增殖并促进细胞凋亡。SMC4 敲低抑制子宫内膜癌细胞的增殖能力并促进细胞凋亡。SMC4 敲低通过降低其磷酸化水平来促进 FoxO1 反式激活。添加 AS 通过增加 FoxO1 的磷酸化水平来抑制 FoxO1 的活性。FoxO1 活性的抑制逆转了 SMC4 沉默对细胞增殖和凋亡的影响。总之，SMC4沉默通过调节FoxO1活性抑制子宫内膜癌的细胞增殖并促进细胞凋亡。