文章：

lncRNA EMSLR 参与子宫内膜癌的二硫键化及进展

The involvement of lncRNA EMSLR in the disulfidptosis and progression of endometrial carcinoma 

原文发布日期：2025-08-14 

英文摘要：

The incidence of endometrial cancer (EC) continues to rise. Disulfidptosis, a novel form of cell death, may represent a potential therapeutic target in EC. Through bioinformatic analysis of The Cancer Genome Atlas (TCGA) database, E2F1 mRNA-stabilizing lncRNA (EMSLR) was identified as a lncRNA related to disulfidptosis in EC. Functional assays, including cell proliferation and xenograft assays, demonstrated that knockdown of EMSLR significantly impeded EC cell proliferation, whereas overexpression of EMSLR promoted cell viability. Additionally, EMSLR was found to be associated with glucose uptake and NADPH production in glucose-restricted culture conditions. Moreover, downregulation of EMSLR markedly increased cell death and induced cytoskeletal collapse under glucose deprivation, as evidenced by F-actin and cell death staining. Notably, we observed a strong correlation between EMSLR and the c-MYC-GLUT1 pathway. Mechanistically, EMSLR was found to mediate the expression and nuclear translocation of c-MYC, thereby regulating the progression of EC and its associated disulfidptosis. In conclusion, EMSLR is identified as a disulfidptosis-related gene in endometrial cancer. Elucidating the function and molecular mechanisms of EMSLR in EC presents a promising avenue for therapeutic intervention in patients. 

摘要翻译：

子宫内膜癌（EC）的发病率持续上升。二硫化物死亡（disulfidptosis）作为一种新型细胞死亡形式，可能成为EC的潜在治疗靶点。通过对癌症基因组图谱（TCGA）数据库进行生物信息学分析，研究发现E2F1 mRNA稳定长链非编码RNA（EMSLR）是与EC二硫化物死亡相关的lncRNA。功能实验（包括细胞增殖和异种移植实验）表明，敲低EMSLR可显著抑制EC细胞增殖，而过表达EMSLR则促进细胞活力。此外，在葡萄糖限制培养条件下，EMSLR与葡萄糖摄取和NADPH生成相关。更重要的是，在葡萄糖剥夺条件下，下调EMSLR会显著增加细胞死亡并诱导细胞骨架崩溃（通过F-肌动蛋白和细胞死亡染色证实）。值得注意的是，我们观察到EMSLR与c-MYC-GLUT1通路之间存在强相关性。从机制上讲，EMSLR介导c-MYC的表达和核转位，从而调控EC进展及其相关二硫化物死亡过程。综上所述，EMSLR被确定为子宫内膜癌中二硫化物死亡相关基因。阐明EMSLR在EC中的功能和分子机制，为患者治疗干预提供了新方向。

原文链接：

The involvement of lncRNA EMSLR in the disulfidptosis and progression of endometrial carcinoma