循环RNAZFR通过miR-624-3p/WEE1轴促进肝细胞癌细胞增殖和上皮细胞-介质细胞过渡过程
1Department of General Surgery, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, China.
概括
肝细胞癌 (HCC) 的进展是由circZFR驱动的,它 sponsesmiR-624-3p以调节WEE1.1. 沉默circZFR抑制HCC的生长,提供了一个潜在的治疗标.
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:
- 肝细胞癌 (HCC) 是全球癌症死亡的主要原因.
- 循环RNAZFR (circZFR) 表达在HCC中升高,但其作用尚不清楚.
研究的目的:
- 阐明HCC中circZFR的分子机制.
- 研究circZFR/miR-624-3p/WEE1轴作为HCC的治疗点的潜力.
主要方法:
- 定量逆转录酶聚合酶连锁反应 (qRT-PCR) 用于基因表达分析.
- 在体外测试 (殖民地形成,繁殖,亡,迁移,入侵) 和西部抹迹.
- 双 luciferase 记者和RNA 免疫沉测试以验证分子相互作用.
- 异种移植模型以评估体内疗效.
主要成果:
- 在circZFR和WEE1上调,而在HCC中miR-624-3p下调.
- circZFR作为miR-624-3p的分子海绵,调节WEE1的表达.
- 击败circZFR抑制了HCC细胞的增殖,迁移和入侵,并促进了细胞亡.
- 在活体中,circZFR敲击抑制了瘤生长.
结论:
- circZFR通过调节miR-624-3p/WEE1轴来促进HCC的进展.
- 这种circZFR/miR-624-3p/WEE1通路代表了HCC治疗的有前途的治疗标.
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