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阿斯坦丁通过调节DNA甲基化,增加瘤抑制基因表达,并通过调节口腔失生性角质细胞中的细胞生物学行为

Peiyan Wang^1,2, Xiaofei Yu^1,2, Pei Sun^1,2

¹Department of Stomatology, The Affiliated Hospital of Qingdao University, Qingdao, China.

Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology

|December 13, 2024

概括

阿斯塔山丁可以降低口腔发育不良症的瘤抑制基因促进基因甲基化,抑制细胞活力和迁移. 这项研究澄清了阿斯塔克桑丁的含量.

科学领域:

口腔瘤学在口腔瘤学.
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
营养生物化学营养生物化学

背景情况:

异常的DNA甲基化在口腔潜在恶性疾病 (OPMDs) 中使瘤抑制基因 (TSGs) 失活.
胡卜素,如阿斯塔丁,通过调节DNA甲基化,在OPMD和口腔状细胞癌 (OSCC) 中显示治疗潜力.

研究的目的:

研究阿斯塔克桑丁抗癌作用与其在OPMD中的DNA甲基化调节能力之间的关系.
阐明阿斯塔克桑丁对口腔失塑性角质细胞 (DOK) 细胞的作用背后的分子机制.

主要方法:

全基因组双硫酸盐测序 (WGBS) 用于全面的DNA甲基化分析.
甲基化特异性PCR,qRT-PCR和西部斑点来评估基因和蛋白质的表达.
细胞活力 (CCK8),迁移 (划伤试验),细胞循环和细胞亡试验,以评估细胞对阿斯塔丁的反应.

主要成果:

在DOK细胞中,WGBS在TSG HOXA3和SOX1中发现了显著的促进物CpG甲基化差异.
阿斯塔克桑丁治疗 (8μM) 减少了这些TSG的促进物CpG甲基化,导致基因表达的增加.
阿斯坦丁抑制了DOK细胞活力,减少了迁移,诱导了G0/G1细胞周期停止,并促进了细胞亡.

结论:

在正常,不形成性和癌症口腔细胞之间存在DNA甲基化模式的显著差异.
阿斯塔山丁降低了DNA甲基转移酶1 (DNMT1) 蛋白质表达的调节,减少了TSG促进剂CpG的甲基化.
阿斯塔ξαν丁通过上调TSG表达来调节DOK细胞的生物行为,为OPMDs提供治疗潜力.

关键词:

通过DNA甲基化.这是一种阿斯塔克桑.口腔潜在的恶性疾病.瘤抑制基因的基因抑制器

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