通过 lncRNA PCAT19 驱动前列腺癌的风险SNP介导促进剂增强剂切换
Junjie Tony Hua1, Musaddeque Ahmed2, Haiyang Guo2
1Princess Margaret Cancer Center, University Health Network, Toronto, ON M5G 1L7, Canada; Department of Medical Biophysics, University of Toronto, Toronto, ON M5G 2M9, Canada.
Cell
|July 24, 2018
概括
一种前列腺癌 (PCa) 风险SNP改变长非编码RNAPCAT19表达,通过一种新的促进剂-增强剂切换机制促进瘤的侵袭性生长和转移.
科学领域:
- 遗传学
- 分子生物学
- 癌症研究
背景情况:
- 与前列腺癌 (PCa) 风险相关的单核酸多态 (SNP) 可以影响疾病的攻击性.
- 长非编码RNAs (lncRNAs) 在癌症的发展和进展中起着关键作用.
研究的目的:
- 阐明PCa风险SNP rs11672691在调节PCAT19表达中的功能机制及其对PCa攻击性的影响.
- 研究PCAT19异型在PCa进展中的作用.
主要方法:
- 对PCAT19异型体进行SNP映射和表达分析.
- 报告者测试以评估促销者和增强者的活动.
- 研究转录因子结合和蛋白质相互作用.
- 与细胞周期和PCa进展相关的基因表达的分析.
主要成果:
- PCa风险SNP rs11672691位于PCAT19-短的促进体中,影响PCAT19-短和PCAT19-长的表达.
- 这种风险变体改变了转录因子的结合,导致促进剂活性降低,增强剂活性增加,从而上调PCAT19-long.
- PCAT19-long与HNRNPAB相互作用,激活细胞循环基因,促进PCa瘤的生长和转移.
结论:
- 通过SNP介导的新型风险促进剂-增强剂切换机制调节PCAT19异型.
- 这种机制有助于前列腺癌的发病和进展.
- PCAT19-long成为促进PCa攻击性的关键参与者.
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