长非编码RNAAC245100.4激活PI3K/AKT通路,通过提高PAR2来促进PCa细胞的增殖
Ke Zhang1, Chi Liu1, Changbin Hu1,2
1Department of Biochemistry & Molecular Biology, Harbin Medical University, Harbin, Heilongjiang, 150086, China.
Heliyon
|June 22, 2023
概括
长非编码RNA AC245100.4 通过激活 PAR2/PI3K/AKT 途径,促进前列腺癌细胞的增殖. 这一发现将AC245100.4确定为前列腺癌的潜在治疗点.
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:
- 前列腺癌 (PCa) 是男性普遍存在的恶性瘤.
- 长非编码RNA (lncRNA) AC245100.4与PCa发展有关.
- 在PCa中AC245100.4的确切机制尚不清楚.
研究的目的:
- 研究AC245100.4在PCa细胞增殖中的作用.
- 阐明PCa中AC245100.4的潜在分子机制.
主要方法:
- 定量逆转录PCR (qRT-PCR) 用于AC245100.4表达.
- RNA免疫沉,然后进行质谱测量 (RAP-MS) 以确定途径.
- 细胞计数工具-8和殖民地形成测试用于增殖.
- 在蛋白质表达 (PAR2,AKT,p-AKT,Cyclin D1,PCNA) 方面进行西式涂抹.
主要成果:
- AC245100.4和PAR2的过度表达增强了PCa细胞的增殖;敲击产生了相反的效果.
- PAR2被确定为AC245100的直接下游目标.4.4.
- AC245100.4通过PI3K/AKT通路促进PCa的扩散.
- 帕尔2倒置逆转了AC245100.4过度表达对p-AKT水平的影响.
结论:
- AC245100.4通过调节PAR2/PI3K/AKT轴来促进PCa细胞的增殖.
- AC245100.4可能作为新瘤标志物和PCa的治疗标.
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