单细胞和机器学习的整合揭示了操作系统驱动的CCND1促进了皮肤状甲状腺癌中的侵略性表型
Jiaxi Wang1, Qingyi Zhu2, Jingyi Bie3
1Department of Breast and Thyroid Surgery, Renmin Hospital of Wuhan University, Wuhan, China.
Frontiers in immunology
|February 6, 2026
概括
氧化应激通过上调CCND1和SOX4.4瘤基因驱动皮皮甲状腺癌 (PTC) 的进展. 针对CCND1及其相关途径为PTC提供了一个潜在的治疗策略.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 生物信息学是一种生物信息学.
背景情况:
- 乳头甲状腺癌 (PTC) 是最常见的甲状腺癌,全球发病率不断增加.
- 氧化应激 (OS) 与癌症的发展有关,但其在PTC中的特定作用需要进一步阐明.
- 识别与OS相关的生物标志物对于PTC诊断和治疗至关重要.
研究的目的:
- 为了研究氧化应激在乳头甲状腺癌中的作用.
- 为了确定PTC的新型OS相关生物标志物.
- 探索针对PTC中的OS途径的治疗策略.
主要方法:
- 单细胞RNA测序和PTC和正常甲状腺组织的差异基因表达分析.
- 生物信息分析包括WGCNA和用于生物标记物选择的机器学习.
- 使用细胞模型进行体外验证,以评估OS对细胞增殖和基因表达的影响.
主要成果:
- 鉴定出CCND1和SOX4是PTC中关键的瘤基因,促进了扩散,入侵和免疫逃避,它们的表达被OS放大.
- CCND1通过PROS1-AXL途径与M2巨分化有关,而SOX4通过MDK途径与血管生成有关.
- TFF3在PTC表达减少,这表明瘤抑制作用可能通过调节免疫反应和减少OS.
结论:
- CCND1作为PTC中的关键瘤基因,由OS通过PI3K/AKT和MAPK通路驱动,导致细胞增殖.
- SOX4也起到瘤基因的作用,而TFF3则起到潜在的瘤抑制作用,两者都与OS相关.
- 准CCND1及其OS介导的途径为乳头甲状腺癌提供了一个有前途的治疗途径.
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