昂科斯塔丁M诱导细胞癌相关的内皮细胞中的表观遗传重编程
Hieu-Huy Nguyen-Tran1, Thi-Ngoc Nguyen2, Tien Hsu3
1Graduate Institute of Biomedical Sciences, China Medical University-Taiwan, No. 91, Hsueh-Shih Rd, Taichung, 40402, Taiwan. nguyentranhieuhuy@mail.cmu.edu.tw.
Communications biology
|November 6, 2025
概括
昂哥斯塔丁M通过表观遗传变化对内皮细胞进行重新编程,促进清细胞细胞癌 (ccRCC) 的进展. 针对这些表观遗传修饰可以减少瘤生长和转移.
科学领域:
- 分子生物学分子生物学
- 癌症研究 癌症研究
- 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:
- 内皮细胞的变化在癌症中至关重要,但激活机制尚不清楚.
- 来自瘤的哥斯塔丁M诱导血管变化,促进清细胞细胞癌 (ccRCC) 的进展.
- 在ccRCC中哥斯塔丁M作用的确切机制仍然是未知的.
研究的目的:
- 阐明Oncostatin M激活内皮细胞的分子机制.
- 调查表观遗传重编程在可斯塔丁M诱导的ccRCC进展中的作用.
- 评估针对哥斯塔丁M介导的表观遗传变化的治疗策略.
主要方法:
- 在内皮细胞中研究了哥斯塔丁M信号传递.
- 分析了表观遗传修饰,特别是由Oncostatin M.诱导的基因组3 lysine 14乙化 (H3K14ac).
- 使用了体外和体外模型,包括ccRCC小鼠模型 (本土和异种移植).
- 评估了向 lysine acetyltransferase 6B 和 Oncostatin M 中和化的影响.
主要成果:
- 哥斯塔丁M信号调节lysine乙转移酶6B,导致内皮细胞中的H3K14ac增加.
- H3K14ac修改了染色质,调高了参与缺氧,血管生成,炎症和介酶过渡的基因组.
- 在ccRCC模型中,准H3K14ac或Oncostatin M改善了癌前表型,并减少了瘤生长和转移.
结论:
- 昂哥斯塔丁M通过氨酸转移酶6B和H3K14ac.激发内皮细胞表观遗传重编程.
- 这种表观遗传重编程驱动了与ccRCC中的前瘤性过程相关的基因表达.
- 干扰这种途径为ccRCC提供了潜在的治疗策略.
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