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在OSCC中阿波利波蛋白D下调:多数据库验证和临床意义
Shuting Wang1,2, Jun Zhao3,4, Rui Bai5,6
1Department of Oral and Maxillofacial Surgery, College & Hospital of Stomatology, Guangxi Medical University, No. 10 Shuangyong Road, Nanning, Guangxi, 530021, China. 202310199@sr.gxmu.edu.cn.
BMC medical genomics
|March 11, 2026
概括
脂蛋白D (APOD) 在口腔状细胞癌 (OSCC) 中显著降低,显示出作为诊断生物标志物的潜力. 它的下调可能会通过破坏I型干扰素-JAK-STAT通路来推动OSCC的进展.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 脂蛋白D (APOD) 是脂素超级家族的成员,参与了亡,癌症和神经修复.
- 虽然APOD在各种癌症中的作用是已知的,但其在口腔状细胞癌 (OSCC) 中的意义尚未得到研究.
研究的目的:
- 调查OSCC中APOD的表达水平和临床意义.
- 探索APOD作为OSCC的诊断和预后生物标志物的潜力.
主要方法:
- 利用来自TCGA,GEO和CPTAC数据库的多omics数据进行APOD mRNA和蛋白质分析.
- 在OSCC组织样本上使用qRT-PCR和免疫组织化学验证的结果.
- 通过sROC曲线,卡普兰-梅尔分析和多变量考克斯回归评估了诊断和预后潜力;使用GSEA探索了途径.
主要成果:
- 与正常对照组相比,APOD mRNA和蛋白质在OSCC组织中显著下调,这在临床样本中得到证实.
- APOD显示出作为OSCC诊断生物标志物的潜力; 病态T阶段是一个独立的预后因素.
- GSEA发现APOD与I型干扰素信号正相关,这表明其下调抑制了这种途径,可能促进OSCC的进展.
结论:
- 在OSCC中,APOD的表达显著降低,表明其作为诊断和预后生物标志物的潜力.
- 对APOD的下调可能会通过损害I型干扰素介导的JAK-STAT信号通路来促进OSCC的进展.
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