通过促进CCNE2表达,ELF3过度表达有助于HPV16 E6/E7-不朽化角质细胞的恶性转变
Yingping Zhu1, Wenjuan Yang2, Yulong Zhuang1
1Department of Obstetrics and Gynecology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), P.R. China.
Journal of microbiology and biotechnology
|November 21, 2024
概括
在由人类乳头瘤病毒16型 (HPV16) 驱动的癌症中,ETS转录因子3 (ELF3) 和环素E2 (CCNE2) 的升高调节. 通过增强CCNE2表达,ELF3促进恶性转变,提供潜在的治疗点.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 病毒学 病毒学
背景情况:
- 持续感染人类乳头瘤病毒16型 (HPV16) 是癌症的重要原因.
- 需要进一步研究HPV16coproteinsE6和E7在角质细胞恶性转变中的作用.
- ETS转录因子3 (ELF3) 和环林E2 (CCNE2) 被确定为HPV16相关癌症的上调调节因子.
研究的目的:
- 为了阐明ELF3和CCNE2在HPV16诱导的恶性转变中的相互作用.
- 调查ELF3在HPV16驱动癌症进展中的功能作用.
- 探索ELF3作为HPV16相关恶性瘤的潜在治疗标.
主要方法:
- 对ELF3和CCNE2的基因表达特征和结合部位的生物信息分析2.
- 使用编码为HPV16 E6和E7.6的逆转录病毒进行人前皮角质细胞 (HFKs) 的体外不朽化.
- 双 luciferase 记者测定证实了 ELF3 和 CCNE2 的相互作用.
- 细胞测定包括CCK-8,细胞循环分析和西部斑点,以评估ELF3功能.
主要成果:
- 在头部和部状细胞癌中,ELF3和CCNE2过度表达.
- 在HFK中HPV16 E6/E7表达导致细胞活力增加,细胞循环加速,ELF3和CCNE2水平升高.
- 过度表达ELF3增强了CCNE2促进者的活性.
- 沉默ELF3抑制了增殖,诱导细胞循环停止,并减少了CCNE2,E6和E7表达在HPV16 E6/E7不朽化HFKs.
结论:
- 低调ELF3抑制了HPV16 E6/E7不朽化HFKs的恶性转变.
- 通过增加CCNE2表达,ELF3促进HPV16驱动的致癌.
- 向ELF3可能是HPV16相关癌症的新疗法策略.
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