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长非编码RNA 02298 通过向miR-28-5p/CCDC6通路促进HC的恶性病变

Jinyi Wang^1,2, Bin Xu^1,2, Litao Liang^1,2

¹Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences, NHC Key Laboratory of Living Donor Liver Transplantation (Nanjing Medical University), Nanjing, 210019, Jiangsu, China.

Biochemical genetics

|February 21, 2024

概括

长非编码RNA LINC02298通过调节miR-28-5p/CCDC6轴促进肝细胞癌 (HCC) 的进展. 这项研究揭示了LINC02298作为HCC的潜在治疗点,影响了扩散,迁移和上皮-介质酶过渡.

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:

肝细胞癌 (HCC) 是一种具有高死亡率的致命恶性瘤.
长非编码RNAs (lncRNAs) 越来越多地被认为是它们在HCC中的调节作用.
LINC02298在HCC病变发生中的特定作用以前是未定义的.

研究的目的:

研究LINC02298在HCC中的表达和功能.
阐明LINC02298在HCC进展中的作用背后的分子机制.
探索LINC02298/miR-28-5p/CCDC6轴在HCC病变发生过程中的作用.

主要方法:

实时定量PCR (RT-qPCR) 用于表达式分析.
在体外测试 (殖民地形成,CCK8,Transwell,EDU,细胞周期,细胞亡) 来评估HCC细胞的行为.
对于表皮层-介质细胞过渡 (EMT) 标记物的西部涂抹.
双露西法酶记者测定,救援实验以验证分子相互作用.

主要成果:

在HCC组织和细胞中,LINC02298的调节显著上升,与预后不佳相关.
过度表达LINC02298促进了HCC细胞的增殖,迁移,入侵和EMT,同时抑制了细胞亡.
LINC02298直接使miR-28-5p成为海绵,导致CCDC6的上调,从而促进HCC恶性病变和EMT.

结论:

LINC02298通过调节miR-28-5p/CCDC6轴,在HCC中充当瘤基因.
LINC02298通过这种分子途径促进HCC进展和EMT.
LINC02298代表了HCC治疗的潜在治疗标.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.在EMT中,EMT是EMT.肝细胞癌是肝细胞癌.这是入侵.在这里,我们可以找到LINC0229898的链接.移民移民移民核武器的扩散

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