MIR222HG/LIN28B/ATG5轴驱动M2巨噬细胞极化和肝癌细胞增殖

IF 1.5 4区 医学 Q4 BIOTECHNOLOGY & APPLIED MICROBIOLOGY
Xiao Zuo, Yan Shao, Yuhang Liang, Chenglong Huo, Shuai Wang
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引用次数: 0

摘要

长链非编码rna (lncRNAs)参与肝细胞癌(HCC)的发病机制。本研究旨在探讨MIR222HG在HCC中的潜力。HCC细胞与U937细胞共培养。采用RT-qPCR和western blot检测基因表达。使用CCK-8、菌落形成和流式细胞术进行功能分析。我们发现MIR222HG在HCC患者以及HepG2和Huh7细胞中过表达。MIR222HG过表达促进肿瘤细胞自噬和m2样肿瘤相关巨噬细胞(TAM2)的激活。此外,mir222hg介导TAM2的激活可促进HCC细胞的增殖。此外,MIR222HG通过与LIN28B结合,增加了ATG5 mRNA的表达,促进了ATG5 mRNA的稳定性。综上所述,mir222hg介导的自噬和TAM2的激活通过调节LIN28B/ATG5信号通路促进HCC细胞的侵袭性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
MIR222HG/LIN28B/ATG5 axis drives M2 macrophage polarization and proliferation of hepatocellular carcinoma cells
Long non-coding RNAs (lncRNAs) are involved in the pathogenesis of hepatocellular carcinoma (HCC). This study aimed to investigated the potentials of MIR222HG in HCC. HCC cells were co-cultured with U937 cells. Gene expression was determined using RT-qPCR and western blot. Functional analysis was performed using CCK-8, colony formation, and flow cytometry assays. We found that MIR222HG was overexpressed in HCC patients as well as HepG2 and Huh7 cells. Overexpressed MIR222HG promoted tumor cell autophagy and the activation of M2-like tumor-associated macrophages (TAM2). Moreover, MIR222HG-mediated the activation of TAM2 drove the proliferation of HCC cells. Additionally, MIR222HG increased the mRNA expression as well as promoted the mRNA stability of ATG5 via binding to LIN28B. In conclusion, MIR222HG-mediated autophagy and the activation of TAM2 promote the aggressiveness of HCC cells via regulating LIN28B/ATG5 signaling.
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来源期刊
Critical Reviews in Eukaryotic Gene Expression
Critical Reviews in Eukaryotic Gene Expression 生物-生物工程与应用微生物
CiteScore
2.70
自引率
0.00%
发文量
67
审稿时长
1 months
期刊介绍: Critical ReviewsTM in Eukaryotic Gene Expression presents timely concepts and experimental approaches that are contributing to rapid advances in our mechanistic understanding of gene regulation, organization, and structure within the contexts of biological control and the diagnosis/treatment of disease. The journal provides in-depth critical reviews, on well-defined topics of immediate interest, written by recognized specialists in the field. Extensive literature citations provide a comprehensive information resource. Reviews are developed from an historical perspective and suggest directions that can be anticipated. Strengths as well as limitations of methodologies and experimental strategies are considered.
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