双A通过GABBR1-介导的MAPK信号传递和巨细胞极化促进OSCC的进展:基于网络毒理学的研究
Qixuan He1, Anquan Ma1, Ziqing Yang1
1Department of Implantology, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Research Center of Dental Materials and Oral Tissue Regeneration & Shandong Provincial Clinical Research Center for Oral Diseases, No.44-1 Wenhua Road West, 250012, Jinan, Shandong, China.
Ecotoxicology and environmental safety
|August 8, 2025
概括
双A (BPA) 通过激活GABBR1信号和通过外体细胞改变瘤微环境来促进口腔癌. GABBR1是BPA诱导的口腔状细胞癌 (OSCC) 的潜在治疗标.
科学领域:
- 在瘤学瘤学.
- 环境健康 环境健康
- 分子生物学分子生物学
背景情况:
- 双甲 (BPA) 是一种环境污染物,与口腔状细胞癌 (OSCC) 的进展有关.
- 在OSCC恶性瘤中BPA作用的精确分子机制尚未完全理解.
- 这项研究调查了GABBR1对BPA诱导的OSCC的参与.
研究的目的:
- 阐明GABBR1在BPA引起的OSCC中的作用.
- 探索BPA对OSCC的影响所涉及的分子通路和细胞相互作用.
- 确定GABBR1作为OSCC的潜在治疗点.
主要方法:
- 生物信息学分析使用TCGA,GTEx和HPA数据库在OSCC中确定了GABBR1.
- 分子对接和模拟评估了BPA-GABBR1相互作用.
- 功能性测试 (西部斑,CCK-8,EDU,transwell) 和外体分析评估了BPA和GABBR1的淘汰效应.
主要成果:
- 通过GABBR1/MEK/ERK通路,BPA暴露增加了OSCC的扩散,迁移,入侵和茎状.
- 通过外体沟通,BPA诱导了M2巨细胞的两极分化,创造了一个免疫抑制的微环境.
- GABBR1表达与OSCC进展相关.
结论:
- 通过GABBR1-介导的信号传递和外体细胞驱动的免疫调节,BPA促进OSCC的进展.
- 在BPA诱导的OSCC恶性瘤中,GABR1发挥着关键作用.
- GABBR1代表了与BPA相关的OSCC的一个有前途的治疗标.
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