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水管烟雾诱导的N6-甲基氨酸修饰促进了口腔状细胞癌的进展

Prathibha Prasad¹, Mohamed Jaber², Al Moutassem Billah Khair³

¹Basic Medical and Dental Sciences Department, College of Dentistry, Ajman University, Ajman, United Arab Emirates; Center for Medical and Bio-Allied Health Sciences Research, Ajman University, Ajman United Arab Emirates; Department of Oral Pathology, Saveetha Dental College and Hospital, Saveetha Institute of Medical and Technical Sciences (SIMATS), Saveetha University, Chennai, India.

International dental journal

|November 30, 2025

概括

水管吸烟通过增加METTL3来促进口腔癌,METTL3驱动HMGA2表达和上皮-介质酶过渡 (EMT). 向METTL3可能为与吸烟相关的口腔状细胞癌 (OSCC) 提供一种新疗法.

科学领域:

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

背景情况:

水管吸烟 (WPS) 是口腔状细胞癌 (OSCC) 的风险因素.
连接WPS与OSCC的分子机制尚未完全理解.
由METTL3调节的m6ARNA甲基化与癌症的发展有关.

研究的目的:

研究暴露在水管烟雾凝结物 (WPSC) 的OSCC细胞中的METTL3表达.
确定METTL3对表皮层-介质酶转换 (EMT) 和OSCC中的增殖的影响.
评估METTL3作为吸烟相关的OSCC的潜在生物标志物和治疗标.

主要方法:

使用WPSC处理了OSCC细胞 (CAL27).
定量PCR和西式涂抹分析了基因和蛋白质表达 (METTL3,HMGA2,EMT标志物).
功能性测试包括细胞增殖,克隆原性测试和METTL3抑制;患者组织和TCGA-OSCC数据集用于验证.

主要成果:

在OSCC细胞中,WPSC治疗显著上调了METTL3,HMGA2和EMT标志物 (P<.001).
抑制METTL3抑制了WPSC诱导的HMGA2表达,EMT和克隆基因潜力.
在患者组织和TCGA数据中,高METTL3表达与转移性和吸烟相关的OSCC相关 (P < .001).

结论:

通过对METTL3进行上调,WPSC促进了OSCC的进展,从而增加了HMGA2表达和EMT.
抑制METTL3表明了治疗潜力.
METTL3作为转移性,与烟草有关的OSCC的潜在生物标志物和治疗标.

关键词:

皮质 - 介质细胞过渡.医疗保健医疗保健医疗保健医疗保健口腔状细胞癌的癌症.通过RNA甲基化.管道烟雾凝结物是水管中的烟雾凝结物.

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