Ovarian cancer (OC) is a deadly disease with limited treatment options and poor overall survival rates. This study aimed to investigate the role of histone modification‐related genes in predicting the prognosis of OC patients. Transcriptome data from multiple cohorts, including bulk RNA‐Seq data and single‐cell scRNA‐Seq data, were collected. Gene set enrichment analysis was used to identify enriched gene sets in the histone modification pathway. Differentially expressed genes (DEGs) between histone modification‐high and histone modification‐low groups were identified using Lasso regression. A prognostic model was constructed using five selected prognostic genes from the DEGs in the TCGA‐OV cohort. The study found enrichment of gene sets in the histone modification pathway and identified five prognostic genes associated with OC prognosis. The constructed risk score model based on histone modification‐related genes was correlated with immune infiltration of T cells and M1 macrophages. Mutations are more prevalent in the high‐risk group compared to the low‐risk group. Several drugs were screened against the model genes. Through in vitro experiments, we confirmed the expression patterns of the model genes. LBX2 facilitates the proliferation of OC. Histone modification‐related genes have the potential to serve as biomarkers for predicting OC prognosis. Targeting these genes may lead to the development of more effective therapies for OC. Additionally, LBX2 represents a novel cell proliferation promoter in OC carcinogenesis.

中文翻译：

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组蛋白修饰相关的卵巢癌预后模型揭示 LBX2 作为一种新型生长促进剂

卵巢癌（OC）是一种致命的疾病，治疗选择有限，总体生存率很低。本研究旨在探讨组蛋白修饰相关基因在预测 OC 患者预后中的作用。收集了来自多个队列的转录组数据，包括批量 RNA-Seq 数据和单细胞 scRNA-Seq 数据。基因集富集分析用于识别组蛋白修饰途径中富集的基因集。使用 Lasso 回归鉴定了组蛋白修饰高组和组蛋白修饰低组之间的差异表达基因 (DEG)。使用来自 TCGA-OV 队列中 DEG 的五个选定的预后基因构建了预后模型。该研究发现组蛋白修饰途径中基因组的富集，并确定了与 OC 预后相关的 5 个预后基因。基于组蛋白修饰相关基因构建的风险评分模型与T细胞和M1巨噬细胞的免疫浸润相关。与低风险组相比，高风险组中的突变更为普遍。针对模型基因筛选了几种药物。通过体外实验，我们证实了模型基因的表达模式。 LBX2 促进 OC 增殖。组蛋白修饰相关基因有潜力作为预测 OC 预后的生物标志物。针对这些基因可能会导致开发出更有效的 OC 疗法。此外，LBX2 是 OC 致癌过程中的一种新型细胞增殖促进剂。