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在HPV阴性患者头部和部状细胞癌中的SP1基因甲基化

Enar Jumaniyazova¹, Anna Aghajanyan¹, Sergey Kurevlev¹

¹Institute of Medicine, Peoples' Friendship University of Russia (RUDN University), 6 Miklukho-Maklaya Street, 117198 Moscow, Russia.

|March 28, 2024

概括

头支状细胞癌 (HNSCC) 的异常DNA甲基化影响SP1基因表达,阻碍了增殖调节. 这种甲基化可以作为HPV阴性HNSCC恶性生长的生物标志物.

科学领域:

表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
分子生物学分子生物学
在瘤学瘤学.

背景情况:

表观遗传机制,特别是DNA甲基化,在致癌过程中对基因表达起着至关重要的作用.
头部和部状细胞癌 (HNSCC) 为研究活跃的增殖性瘤细胞中异常DNA甲基化提供了一个模型.
了解这些机制对于识别新生物标志物和治疗点至关重要.

研究的目的:

研究瘤组织中特定基因 (CDKN1,CDKN2A,MYC,Smad3,SP1,UBC) 的甲基化状态,与HPV阴性HNSCC患者的正常组织相比.
探索SP1基因甲基化与HNSCC特征之间的相关性,包括瘤类型,阶段,年龄和吸烟状况.
评估DNA甲基化作为HNSCC生物标志物的潜力.

主要方法:

利用双硫酸盐转化和甲基敏感的高分辨率化曲线分析来量化基因甲基化.
分析了来自50名被诊断为HPV阴性HNSCC的患者的瘤和相邻正常组织样本.
检查了各种患者亚组的甲基化水平 (舌头,喉,其他癌症;T2-T4阶段;年龄<50岁和>50岁;吸烟者和非吸烟者).

主要成果:

在所有患者和子组中,在瘤DNA和正常DNA之间观察到SP1基因甲基化水平的持续差异.
发现瘤DNA中SP1基因的甲基化抑制了它的表达.
这种抑制SP1表达阻碍了HNSCC细胞增殖的调节.

结论:

在HNSCC瘤DNA中SP1基因甲基化抑制了基因表达,损害了增殖控制,并可能表明恶性细胞生长.
异常的DNA甲基化模式,特别是高甲基化促进体,作为HNSCC的潜在生物标志物具有前景.
对癌症发生过程中的DNA甲基化进行进一步的研究可以带来更好的诊断和预后工具.

关键词:

这就是Sp1基因.表观遗传变化表观遗传变化头部和部状细胞癌状细胞癌甲基化DNA的DNA的甲基化.

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