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长非编码RNA X-无活性特异转录 通过微RNA 34a/指 E-box-binding Homeobox 1路径促进食道状细胞癌的进展
Bin Guo1, Ming He1, Minting Ma2
1Department of Thoracic Surgery, Fourth Hospital of Hebei Medical University, 12 Jiankang Road, Chang'an District, Shijiazhuang, 050011, Hebei, China.
Digestive diseases and sciences
|February 17, 2024
概括
长非编码RNAXIST通过调节ZEB1并通过miR-34a通路抑制E-cadherin,促进食道状细胞癌 (ESCC) 的进展. 针对这个XIST/miR-34a/ZEB1轴可能为ESCC提供治疗策略.
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:
- 长非编码RNAXIST对于X染色体沉默至关重要.
- 指 E-box-binding homeobox 1 (ZEB1) 调节了上皮细胞-介质细胞过渡 (EMT). 指 E-box-binding homeobox 1 (ZEB1) 调节了上皮细胞-介质细胞过渡 (EMT).
研究的目的:
- 研究XIST在食道状细胞癌 (ESCC) 进展中的作用.
- 阐明涉及miR-34a/ZEB1/E-cadherin/EMT通路的机制.
主要方法:
- 通过qPCR和免疫组织化学分析了XIST和ZE1的表达.
- 在ESCC细胞 (KYSE150) 中使用siRNA/shRNA.执行XIST敲除.
- 评估了细胞增殖,迁移,入侵和体内瘤生长.
- 使用 luciferase 记者测定来确认分子相互作用.
主要成果:
- 在ESCC组织中,XIST和ZEB1的调节升高,与预后不佳相关.
- 通过XIST knockdown抑制了ESCC细胞的增殖,迁移和入侵.
- 通过XIST敲击降低了ZEB1,增加了E-cadherin和miR-34a水平,证实了途径的参与.
- 在体内,XIST knockdown抑制了异种移植瘤的生长.
结论:
- 通过miR-34a/ZEB1/E-cadherin/EMT通路,XIST驱动ESCC的进展.
- XIST/miR-34a/ZEB1轴为ESCC提供了一个潜在的治疗标和预后生物标志物.
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