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转录因子FOXP4反向控制瘤抑制基因,并有助于甲状腺癌的进展
Tian Zhou1,2, Ning Ma1,3, Yong-Lin Zhang2
1School of Clinical Medicine, Guizhou Medical University, Guiyang, 550001, Guizhou, China.
Heliyon
|January 31, 2024
概括
增加的FOXP4水平通过抑制FBXW7.7驱动甲状腺癌 (TC) 的进展. 恢复FBXW7表达抑制TC细胞生长和恶性表型,为这种不断增长的癌症提供潜在的治疗标.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 遗传学 是一个遗传学.
背景情况:
- 甲状腺癌 (TC) 的发病率在全球范围内正在增加.
- 转录因子FOXP4与各种癌症有关,但其在TC中的作用尚不清楚.
- 了解FOXP4在TC中的功能对于开发向疗法至关重要.
研究的目的:
- 研究转录因子FOXP4在甲状腺癌中的作用.
- 在TC中阐明FOXP4与其目标基因FBXW7之间的功能关系.
- 确定FOXP4和FBXW7对TC细胞行为和瘤生长的影响.
主要方法:
- 在TC组织和细胞系中使用免疫组织化学和RT-qPCR评估FOXP4和FBXW7表达.
- 研究了FOXP4对细胞增殖,迁移,细胞循环和上皮-介质细胞过渡 (EMT) 的影响.
- 通过ChIP测定证实了FOXP4-FBXW7相互作用,并评估了FBXW7对体外和体内FOXP4驱动的表型的影响.
主要成果:
- 较高的FOXP4水平和较低的FBXW7水平与侵袭性乳头甲状腺癌相关.
- 过度表达FOXP4促进了TC细胞的增殖,迁移和EMT.
- FOXP4直接抑制了FBXW7的转录;FBXW7的恢复抵消了FOXP4的影响.
- 在体内,FOXP4的淘汰减少了瘤的生长,并增加了FBXW7水平.
结论:
- 在甲状腺癌中,FOXP4充当FBXW7转录的关键调节者.
- 由FOXP4驱动的异常FBXW7表达有助于攻击性TC中的恶性表型.
- 准FOXP4-FBXW7轴可能为甲状腺癌提供一种新的治疗策略.
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