SMYD3-CDCP1轴在结肠直肠癌中驱动EMT和CAF激活,并且可以针对氧沙敏化
Liming Zhao1,2, Zhexue Wang1, Pu Cheng1
1Department of Colorectal Surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, No. 17 South Lane of Panjiayuan, Chaoyang District, Beijing 100020, China.
Biomedicines
|November 27, 2025
概括
SMYD3-CDCP1通路在表观遗传上驱动着结直肠癌的进展和转移. 准这一轴可能会改善化疗反应并减少CRC的传播.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
背景情况:
- 大肠直肠癌 (CRC) 的死亡率源于肝转移和化疗耐药性.
- 基因组甲基转移酶SMYD3在CRC进展中的作用及其下游目标仍然难以捉摸.
研究的目的:
- 在结直肠癌中研究SMYD3-CDCP1轴.
- 确定SMYD3对CDCP1转录的调节及其对瘤微环境和化疗敏感性的影响.
主要方法:
- 使用了ChIP-qPCR,西式涂抹和共同培养实验.
- 评估了SMYD3-CDCP1轴对上皮层-介质细胞过渡 (EMT),癌症相关纤维细胞 (CAF) 激活和氧化 (OXA) 敏感性的影响.
主要成果:
- 通过H3K4me3丰富,SMYD3直接增强了CDCP1转录.
- 调节后的CDCP1促进了EMT和CAF的激活,驱动了入侵和 stromal重塑.
- 抑制SMYD3减少了转移,并在体内改善了OXA反应;向SMYD3提高了体内OXA的敏感性.
结论:
- SMYD3-CDCP1轴在表观遗传上通过促进CDCP1转录和重塑瘤微环境来驱动CRC进展.
- 针对SMYD3-CDCP1通路为CRC转移和化疗耐药性提供了潜在的治疗策略.
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