MIR222HG/LIN28B/ATG5 axis drives M2 macrophage polarization and proliferation of hepatocellular carcinoma cells

Abstract

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.