通过准miR-98-5p/PBX3轴,LncRNA LINC00885促进了膀癌的进展
Zongyu Xia1, Qin Wang2, Peng Lu1
1Department of Urology, Chongqing University Three Gorges Hospital, Chongqing 404000, China. zhuji6984479984@163.com.
Cellular and molecular biology (Noisy-le-Grand, France)
|June 10, 2023
概括
长非编码RNA LINC00885通过向miR-98-5p/PBX3通路来促进膀癌 (BLCA) 的进展. LINC00885可以作为BLCA治疗的新生物标志物.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 遗传学 是一个遗传学.
背景情况:
- 膀癌 (BLCA) 是一种普遍存在的恶性瘤,具有显著的死亡率,特别是在男性中.
- 长非编码RNAs (lncRNAs) 越来越多地被认为是它们在瘤发育中的作用.
- 在BLCA中LINC00885的特定功能仍然在很大程度上未被描述.
研究的目的:
- 研究LINC00885在膀癌中的调节作用.
- 阐明LINC00885在BLCA中的功能背后的分子机制.
主要方法:
- 定量实时PCR (qRT-PCR) 用于LINC00885表达式分析.
- 细胞增殖 (CCK-8,殖民地形成) 和细胞灭绝 (caspase-3,西斑) 的测试.
- RNA免疫沉 (RIP) 和RNA下拉试验,以探索LINC00885,miR-98-5p和PBX3.3之间的相互作用.
主要成果:
- 在BLCA组织中,LINC00885表达显著上调.
- 在BLCA细胞中,LINC00885的过度表达促进了细胞增殖和抑制了细胞亡.
- LINC00885通过菌miR-98-5p作为竞争的内源RNA (ceRNA) 起作用,从而提高PBX3表达的调节.
- miR-98-5p模仿抑制的BLCA细胞增殖和诱导的亡,而LINC00885的过度表达逆转了这些效应.
- 敲除LINC00885抑制了BLCA的进展,并且这种效应被PBX3过度表达部分挽救.
结论:
- 通过miR-98-5p/PBX3轴,LINC00885促进了膀癌的进展.
- LINC00885可能是一个潜在的治疗标和膀癌的诊断生物标志物.
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