Endometrial cancer (EC) is the most common gynecologic malignancy and still remains clinically challenging. We aimed to explore the potential biomarkers of EC and provide a theoretical basis for early screening and targeted therapy. The available transcriptome data from the Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) were analyzed to identify differentially expressed genes. Immunohistochemistry was performed to detect gene expression. We analyzed the associations of MYBL2 with clinicopathological features and survival time and the biological effect of MYBL2 on the proliferation of EC cells. The effect of MYBL2 silencing on the transcriptome of EC cell model was analyzed by RNA-Seq. MYBL2 was significantly upregulated with obvious copy number alteration (CNA) in EC. Copy number amplification significantly increased MYBL2 mRNA expression, which led to a poor prognosis and severe pathological types of EC. Additionally, MYBL2 silencing significantly inhibited proliferation and induced apoptosis and G₁-phase cell cycle arrest in EC cell lines. Our results indicate that MYBL2 is closely related to the cell cycle and apoptosis pathways in EC. The findings in this study provide evidence that MYBL2 can serve as a new candidate prognostic marker and a target for future therapeutic intervention in EC.

子宫内膜癌 (EC) 是最常见的妇科恶性肿瘤，在临床上仍然具有挑战性。我们旨在探索EC的潜在生物标志物，为早期筛查和靶向治疗提供理论基础。分析来自癌症基因组图谱 (TCGA) 和基因表达综合 (GEO) 的可用转录组数据，以确定差异表达的基因。进行免疫组织化学以检测基因表达。我们分析的协会MYBL2与临床病理特征和生存时间和生物效应MYBL2对EC细胞的增殖。的效果MYBL2是由RNA-SEQ分析沉默上EC细胞模型的转录。MYBL2在 EC 中显着上调并伴有明显的拷贝数改变 (CNA)。拷贝数扩增显着增加了MYBL2 mRNA 的表达，导致预后不良和严重的 EC 病理类型。此外，MYBL2沉默显着抑制EC 细胞系中的增殖并诱导细胞凋亡和 G _{1 期}细胞周期停滞。我们的结果表明MYBL2与 EC 中的细胞周期和凋亡途径密切相关。本研究的结果提供证据表明MYBL2可以作为新的候选预后标志物和未来 EC 治疗干预的目标。