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生物信息学方法用于多组学分析CDKN2A作为子宫体子宫内膜癌生物标志物和治疗靶点的潜力。

Bioinformatics approaches to multi-omics analysis of the potential of CDKN2A as a biomarker and therapeutic target for uterine corpus endometrial carcinoma.

作者信息

Ma Liang, Li Yuling, Wu Jingxian, Gao Yanfei

机构信息

Department of Pathology, College of Basic Medicine, Chongqing Medical University, Chongqing, 400000, China.

Biochemistry and Molecular Biology, College of Basic Medical Science, Chongqing Medical University, Chongqing, 400000, China.

出版信息

Sci Rep. 2025 Jan 6;15(1):895. doi: 10.1038/s41598-025-85364-w.

DOI:10.1038/s41598-025-85364-w
PMID:39762354
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11704072/
Abstract

Uterine corpus endometrial carcinoma (UCEC) is a significant cause of cancer-related mortality among women worldwide. Prior research has demonstrated an association between cyclin-dependent kinase inhibitor 2 A (CDKN2A) and various tumors. As a member of the INK4 family, CDKN2A is involved in cell cycle regulation by controlling CDKs. In the present study, bioinformatics was used to analyze public datasets. The expression levels, signaling pathways, and copy number variations of CDKN2A in UCEC were explored, along with its immune cell subset associations. CDKN2A expression was found to be elevated in UCEC, particularly in the signaling pathways involved in cell proliferation and inflammation. Analysis of somatic copy number alterations in the TCGA (The Cancer Genome Atlas)-UCEC dataset revealed a connection between CDKN2A and drug metabolism in UCEC. Assessment of the relationship between CDKN2A and genes involved in immunotherapy for UCEC patients showed a negative correlation between CDKN2A and CD8 T cell activity, as well as IL-2 and TP53. Collectively, these insights suggest that CDKN2A may be a potential biomarker for prognosis and treatment strategies in UCEC.

摘要

子宫体子宫内膜癌(UCEC)是全球女性癌症相关死亡的重要原因。先前的研究表明细胞周期蛋白依赖性激酶抑制剂2A(CDKN2A)与多种肿瘤之间存在关联。作为INK4家族的成员,CDKN2A通过控制细胞周期蛋白依赖性激酶参与细胞周期调控。在本研究中,利用生物信息学分析公共数据集。探讨了UCEC中CDKN2A的表达水平、信号通路、拷贝数变异及其与免疫细胞亚群的关联。发现CDKN2A在UCEC中表达升高,特别是在参与细胞增殖和炎症的信号通路中。对癌症基因组图谱(TCGA)-UCEC数据集中体细胞拷贝数改变的分析揭示了UCEC中CDKN2A与药物代谢之间的联系。评估CDKN2A与UCEC患者免疫治疗相关基因之间的关系,结果显示CDKN2A与CD8 T细胞活性以及白细胞介素-2和TP53呈负相关。总体而言,这些见解表明CDKN2A可能是UCEC预后和治疗策略的潜在生物标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83e9/11704072/cb5a6aa0e9da/41598_2025_85364_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83e9/11704072/e8850897138a/41598_2025_85364_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83e9/11704072/64daca0efa93/41598_2025_85364_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83e9/11704072/718755d4bd06/41598_2025_85364_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83e9/11704072/cb5a6aa0e9da/41598_2025_85364_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83e9/11704072/e8850897138a/41598_2025_85364_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83e9/11704072/a0b18bc296c7/41598_2025_85364_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83e9/11704072/ec8573558d2f/41598_2025_85364_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83e9/11704072/64daca0efa93/41598_2025_85364_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83e9/11704072/718755d4bd06/41598_2025_85364_Fig5_HTML.jpg
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