MIR222HG/LIN28B/ATG5 Axis Drives M2 Macrophage Polarization and Proliferation of Hepatocellular Carcinoma Cells

被引：0

作者：

Zuo, Xiao ^{[1
]}

Shao, Yan ^{[1
]}

Liang, Yuhang ^{[1
]}

Huo, Chenglong ^{[1
]}

Wang, Shuai ^{[1
]}

机构：

[1] Yangtze Univ, Jingzhou Hosp, 26 Chuyuan Ave, Jingzhou 434020, Hubei, Peoples R China

来源：

CRITICAL REVIEWS IN EUKARYOTIC GENE EXPRESSION | 2024年 / 34卷 / 03期

关键词：

hepatocellular carcinoma; MIR222HG; autophagy; M2-like tumor-associated macrophages;

D O I：

10.1615/CritRevEukaryotGeneExpr.2023049637

中图分类号：

Q81 [生物工程学（生物技术）]; Q93 [微生物学];

学科分类号：

071005 ; 0836 ; 090102 ; 100705 ;

摘要：

Long non-coding RNAs (IncRNAs) are involved in the pathogenesis of hepatocellular carcinoma (HCC). This study aimed to investigate the potential of MIR222HG in HCC. HCC cells were co-cultured with U937 cells. Gene expression was determined using reverse transcription-quantitative (RT-q) PCR and western blot. Functional analysis was performed using Cell Counting Kit 8 (CCK-8), colony formation, and flow cytometry assays. We found that MIR222HG was overexpressed in HCC patients as well as HepG2 and Hulh7 cells. MIR222HG-mediated upregulation of autophagy related 5 (ATG5) 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 lin-28 homolog B (LIN28B). In conclusion, MIR222HG-mediated autophagy and the activation of TAM2 promote the aggressiveness of HCC cells via regulating LIN28B/ATG5 signaling

引用

页码：17 / 26

页数：10

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