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条件淘汰赛小鼠模型揭示了百氧化素1在口腔白血病癌症发生中的关键作用
Lingyu Li1, Jing Li2, Yunping Lu3
1Department of Oral Pathology, Beijing Stomatological Hospital & School of Stomatology, Capital Medical University, Beijing, China.
Heliyon
|May 31, 2024
概括
百氧化素1 (Prx1) 促进口腔白血病 (OLK) 致癌的发生. 在小鼠中淘汰Prx1降低了OLK恶性转化和抑制了细胞增殖,这表明Prx1是癌前口腔病变的治疗标.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 遗传学 遗传学 是一个
背景情况:
- 氧化素1 (Prx1) 是一种抗氧化蛋白质,涉及致癌.
- 口腔白血病 (OLK) 是一种具有潜在恶性转变的癌前病变.
- Prx1在OLK发展中的作用需要进一步研究.
研究的目的:
- 为了研究Prx1对OLK的口腔粘膜上皮质的影响.
- 为了生成和验证Prx1条件淘汰赛 (cKO) 鼠标模型.
- 评估Prx1淘汰对OLK发育和进展的影响.
主要方法:
- 使用CRISPR/Cas9和Cre-loxP系统生成一个Prx1 cKO小鼠模型.
- 在小鼠中构建了4-基诺林-1-氧化物 (4NQO) 诱导的OLK模型.
- 用PCR,测序和免疫组织化学进行遗传和蛋白质验证.
- 进行了组织学分析和Ki67免疫染,以评估OLK发生和细胞增殖.
主要成果:
- 成功生成了Prx1 cKO小鼠 (Prx1flox/flox:Cre+) 在舌头上皮质中确认了Prx1删除.
- 在4NQO诱导的OLK中,Prx1淘汰赛显著降低了恶性转变的发生率.
- Prx1 缺乏明显抑制了舌头上皮细胞中的细胞增殖.
- 在Prx1 cKO小鼠的主要器官中没有观察到显著的组织学异常.
结论:
- 开发了一种可靠的Prx1 cKO小鼠模型,用于研究口腔致癌.
- 在促进OLK发展和进步方面,Prx1起着至关重要的作用.
- 向Prx1为癌前口腔病变提供了潜在的治疗策略.
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