MALAT1/mir-1-3p介导的BRF2表达通过抑制LKB1/AMPK信号通路促进HCC的进展
Guang-Zhen Li1,2, Guang-Xiao Meng2,3, Guo-Qiang Pan2,3
1Medical Integration and Practice Center, Cheeloo College of Medicine, Shandong University, Jinan, China.
Cancer cell international
|August 31, 2023
概括
转移相关的肺腺癌转录1 (MALAT1) 通过通过海绵化miR-1-3p对BRF2进行上调来促进肝细胞癌 (HCC). 向MALAT1可抑制HCC进展和瘤生长,提供一种潜在的治疗策略.
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:
- 长非编码RNA转移相关的肺腺癌转录1 (MALAT1) 与各种癌症有关.
- 它在肝细胞癌 (HCC) 中的确切作用和机制尚不完全理解.
研究的目的:
- 阐明MALAT1在HCC中的功能作用和潜在的分子机制.
- 研究MALAT1作为HCC的潜在治疗点.
主要方法:
- 定量实时PCR (qRT-PCR) 用于评估MALAT1的表达.
- 在体外测试 (CCK-8,殖民地形成,Transwell,伤口愈合,流细胞计) 来评估HCC细胞行为.
- 西方涂抹用于蛋白质水平分析 (AMPK,亡相关蛋白质).
- 双露西法酶记者测定以确认RNA相互作用.
主要成果:
- 在HCC组织和细胞系中,MALAT1的表达被上调.
- 抑制MALAT1抑制了HCC细胞的增殖,迁移,入侵,并促进了细胞亡.
- 马拉特1通过海绵化miR-1-3p积极调节BRF2表达,有助于瘤的进展.
- 抑制BRF2激活了LKB1/AMPK通路,抑制了HCC.
- 通过ASO介导的MALAT1抑制减少了异种移植瘤的生长.
结论:
- 在HCC中确定了一个新的调节轴 (MALAT1/miR-1-3p/BRF2/LKB1/AMPK).
- 这一轴代表了HCC治疗的有前途的分子治疗标.
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