リスクSNP媒介のプロモーター強化スイッチングは,IncRNA PCAT19を通じて前立腺がんを誘発する
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
まとめ
前立腺がん (PCa) リスクSNPは,長い非コーディングRNAPCAT19発現を変化させ,新しいプロモーター強化スイッチングメカニズムを通じて,攻撃的な腫瘍の成長と転移を促進します.
科学分野:
- 遺伝学
- 分子生物学
- 癌 研究
背景:
- 前立腺がん (PCa) リスクに関連した単一のヌクレオチドポリモルフィズム (SNPs) は,疾患の攻撃性に影響を与える可能性があります.
- 長い非コーディングRNA (lncRNAs) は,がんの発生と進行において重要な役割を果たします.
研究 の 目的:
- lncRNAのPCAT19発現を調節するPCaリスクSNP rs11672691の機能的メカニズムとそのPCa攻撃性への影響を明らかにする.
- PCAの進行におけるPCAT19アイソフォームの役割を調査する.
主な方法:
- PCAT19イソフォームのSNPマッピングと発現分析
- レポーターアッセイは,プロモーターとエンハンサーの活動を評価するものです.
- 転写因子結合とタンパク質の相互作用の調査
- 細胞サイクルとPCaの進行に関連する遺伝子発現の分析
主要な成果:
- PCaリスクSNP rs11672691はPCAT19-shortのプロモーターにあり,PCAT19-shortとPCAT19-longの両方の発現に影響する.
- リスク変異は転写因子の結合を変化させ,プロモーターの活性が低下し,増強剤の活性が増加し,PCAT19- ロングを上調する.
- PCAT19- ロングはHNRNPABと相互作用して細胞サイクル遺伝子を活性化し,PCa腫瘍の成長と転移を促進します.
結論:
- 新しいリスクSNP媒介のプロモーター強化スイッチングメカニズムはPCAT19イソフォームを調節する.
- このメカニズムは 侵襲的な前立腺がんの発症と進行の両方に寄与します
- PCAT19-longはPCaの攻撃性を促進する重要な役割を果たしている.
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