RNF135 促进人类骨髓瘤细胞生长并通过对PI3K/AKT通路进行上调来抑制细胞亡
Bingyao Chen1,2,3, Yinglong Zhang3, Guangze Song2,3
1Second Department of Orthopedics, Beijing Daxing District People's Hospital, Beijing, China.
Cancer reports (Hoboken, N.J.)
|August 9, 2024
概括
环指蛋白135 (RNF135) 在骨髓瘤 (OS) 中升高,并通过激活PI3K/AKT通路来驱动瘤生长. 抑制RNF135可能为OS患者提供新的治疗策略.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 生物化学 生物化学
背景情况:
- 环指蛋白135 (RNF135) 是一种E3泛基因酶,参与瘤发生.
- 人类骨髓瘤 (OS) 发展中的RNF135的作用以前是未知的.
研究的目的:
- 研究RNF135在人类骨髓瘤中的表达和功能.
- 阐明RNF135在OS中的作用背后的分子机制.
主要方法:
- 免疫组织化学评估RNF135表达在OS和骨质神经瘤组织.
- 在体外研究中,使用shRNA在OS细胞中击败RNF135,评估增殖,亡和酶激活.
- 西部斑点分析以确定PI3K,AKT和p-AKT蛋白水平.
主要成果:
- 与骨质软骨相比,RNF135的表达在骨组织中显著更高.
- RNF135敲击抑制了OS细胞的增殖和诱导的亡.
- 抑制RNF135可以降低PI3K和p-AKT水平,并激活caspase 3和7.
结论:
- RNF135通过PI3K/AKT依赖的途径促进人类骨髓瘤的发展.
- 准RNF135为骨髓瘤提供了一个潜在的治疗策略.
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