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.

中文翻译：

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

长链非编码RNA (lncRNA) 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。使用逆转录定量 (RT-q) PCR 和蛋白质印迹测定基因表达。使用细胞计数试剂盒 8 (CCK-8)、集落形成和流式细胞术分析进行功能分析。我们发现 MIR222HG 在 HCC 患者以及 HepG2 和 Huh7 细胞中过度表达。MIR222HG 介导的自噬相关 5 (ATG5) 上调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介导的TAM2激活驱动HCC细胞的增殖。此外，MIR222HG 通过与 lin-28 同源物 B (LIN28B) 结合增加了 ATG5 的 mRNA 表达并促进了 mRNA 稳定性。总之，MIR222HG 介导的自噬和 TAM2 的激活通过调节 LIN28B/ATG5 信号传导促进 HCC 细胞的侵袭性。