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<p>Hepatitis B virus (HBV) infection remains a leading cause of chronic liver disease and liver failure worldwide. Although miR-148a-3p has been implicated in liver pathophysiology, its specific role in HBV replication through autophagy-related signaling pathways is not fully understood. This study aimed to investigate the effects of miR-148a-3p on HBV transcription and replication, focusing on its regulation of AMPK/mTOR-dependent autophagy. HepG2.2.15 cells were transfected with miR-148a-3p mimics or inhibitors, with or without the AMPK agonist AICAR. HBV replication markers (pgRNA, HBsAg, HBeAg), autophagy-related proteins (LC3, p62, Beclin-1), and AMPK/mTOR/S6 pathway components were analyzed by Western blotting, ELISA, qRT-PCR, and immunofluorescence. Cell viability was measured using the MTT assay at 12–72-h post-transfection. Overexpression of miR-148a-3p increased pgRNA, HBsAg, and HBeAg production (<i>P</i> &lt; 0.01), enhanced autophagy as indicated by elevated Beclin-1 and LC3-II with reduced p62 (<i>P</i> &lt; 0.01), activated AMPK, and inhibited mTOR and S6 phosphorylation (<i>P</i> &lt; 0.01). In contrast, miR-148a-3p knockdown reduced HBV replication and autophagy, effects that were partially reversed by AICAR treatment (<i>P</i> &lt; 0.01). miR-148a-3p promotes HBV transcription and replication by inducing autophagy via AMPK activation and mTOR/S6 suppression. These findings provide mechanistic insight into HBV pathogenesis and identify miR-148a-3p as a potential therapeutic target for regulating HBV replication and autophagy.</p>

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Mechanistic study of miR-148a-3p-mediated AMPK/mTOR/S6-dependent autophagy in hepatitis B virus replication

  • 期刊论文

  • 发表日期：

    2026年1月5日

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  • Juan Liu,
  • Yuanji Sheng

摘要

Hepatitis B virus (HBV) infection remains a leading cause of chronic liver disease and liver failure worldwide. Although miR-148a-3p has been implicated in liver pathophysiology, its specific role in HBV replication through autophagy-related signaling pathways is not fully understood. This study aimed to investigate the effects of miR-148a-3p on HBV transcription and replication, focusing on its regulation of AMPK/mTOR-dependent autophagy. HepG2.2.15 cells were transfected with miR-148a-3p mimics or inhibitors, with or without the AMPK agonist AICAR. HBV replication markers (pgRNA, HBsAg, HBeAg), autophagy-related proteins (LC3, p62, Beclin-1), and AMPK/mTOR/S6 pathway components were analyzed by Western blotting, ELISA, qRT-PCR, and immunofluorescence. Cell viability was measured using the MTT assay at 12–72-h post-transfection. Overexpression of miR-148a-3p increased pgRNA, HBsAg, and HBeAg production (P < 0.01), enhanced autophagy as indicated by elevated Beclin-1 and LC3-II with reduced p62 (P < 0.01), activated AMPK, and inhibited mTOR and S6 phosphorylation (P < 0.01). In contrast, miR-148a-3p knockdown reduced HBV replication and autophagy, effects that were partially reversed by AICAR treatment (P < 0.01). miR-148a-3p promotes HBV transcription and replication by inducing autophagy via AMPK activation and mTOR/S6 suppression. These findings provide mechanistic insight into HBV pathogenesis and identify miR-148a-3p as a potential therapeutic target for regulating HBV replication and autophagy.