在宫癌细胞中,LINC00460通过增强NF-κB介导的VEGFA表达来促进血管生成
Fan Li1, Weipei Zhu2
1Department of Gynecology and Obstetrics, The Second Affiliated Hospital of Soochow University, Suzhou, 215000, China; Department of Gynecology, Shanghai Xuhui Central Hospital, Shanghai, 200031, China; Department of Gynecology, Zhongshan-Xuhui Hospital, Fudan University, Shanghai, 200031, China.
Biochemical and biophysical research communications
|June 11, 2023
概括
长非编码RNA LINC00460通过激活NF-κB-VEGFA通路来促进宫癌血管生成. 这一途径是阻止瘤生长和转移的潜在治疗标.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
背景情况:
- 瘤血管生成对于癌症生长和转移至关重要.
- 像LINC00460这样的长非编码RNA (lncRNAs) 在癌症中具有复杂的作用.
- 在宫癌血管生成中LINC00460的确切功能尚不清楚.
研究的目的:
- 阐明LINC00460在宫癌血管生成中的功能机制.
- 研究LINC00460在调节血管内皮生长因子A (VEGFA) 和NF-κB通路中的作用.
主要方法:
- 使用的条件介质 (CM) 来自LINC00460 - 敲击和过度表达的宫癌细胞.
- 评估人静脉内皮细胞 (HUVEC) 的迁移,入侵和管道形成.
- 研究了VEGFA转录,NF-κB通路激活,以及重组VEGFA的影响.
主要成果:
- LINC00460敲击减弱了HUVEC血管生成,而上调则增强了它.
- 发现LINC00460可以刺激VEGFA转录并激活NF-κB通路.
- 维格法调解了LINC00460.4的亲血管效应.
结论:
- LINC00460通过NF-κB-VEGFA轴促进子宫癌血管生成.
- 准LINC00460-NF-κB-VEGFA通路是一个潜在的策略来抑制瘤血管生成.
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