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

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ID: 278010
2024
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Abstract
Long non-coding RNAs (lncRNAs) 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 Huh7 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.
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zuo2024mir222hglin28batg5critical Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors
Journal Critical reviews in eukaryotic gene expression
Year 2024
DOI
10.1615/CritRevEukaryotGeneExpr.2023049637
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