在口腔上皮细胞中,KSHV和HPV调节了上皮细胞到介质细胞的转换
Qian Li1,2, Sharon E Hopcraft1,2, Philip T Lange1,2
1Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
mBio
|August 15, 2025
概括
卡波西的肉瘤相关性疹病毒 (KSHV) 和人类乳头瘤病毒 (HPV) 通过诱导上皮细胞转化为介质细胞转化 (EMT) 来驱动口腔癌. 向维门丁可以逆转EMT和癌细胞特征,为KSHV和HPV驱动的口腔癌提供潜在的治疗策略.
科学领域:
- 病毒学 病毒学
- 在瘤学瘤学.
- 细胞生物学 细胞生物学
背景情况:
- 口腔癌经常与瘤原人乳头瘤病毒 (HPV) 和疹病毒 (如卡波西的瘤相关疹病毒 (KSHV)) 相关.
- 连接这些病毒感染与口腔癌的发展和进展的确切机制尚未完全阐明.
研究的目的:
- 研究KSHV和HPV31感染在诱导正常口腔角质细胞 (NOKs) 中表皮细胞转化为介质细胞转化 (EMT) 的作用.
- 探索向EMT通路的潜力,特别是维门丁,作为KSHV和HPV相关的口腔癌的治疗策略.
主要方法:
- 通过端粒酶使正常口腔牙角质细胞 (NOKs) 不朽化,后者被KSHV或HPV潜伏感染31.
- 评估表型变化,包括形态,增殖,迁移和入侵.
- 对表皮细胞 (E-cadherin) 和介质细胞 (vimentin) 标记物表达的分析.
- 使用shRNAs和埃里布林治疗来评估EMT逆转.
主要成果:
- 受KSHV和HPV31感染的NOKs表现出纤维细胞样形态,增多增殖,迁移和入侵.
- 受感染的细胞显示E-cadherin的减少和vimentin的增加,表明EMT.
- 维门丁倒置或埃里布林治疗恢复了E-cadherin的表达,并消除了病毒诱导的表型变化.
结论:
- 在口腔上皮细胞中,KSHV和HPV31感染会诱导EMT,从而导致类似癌症的表型.
- 维丁在KSHV和HPV31诱导的EMT和相关的恶性特征中发挥着关键作用.
- 向维门丁代表了对KSHV和HPV驱动的口腔癌的有希望的治疗途径.
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