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<p>Gastric cancer (GC) is the fifth most common malignancy and the fifth highest cause of cancer-related deaths on a global scale. This study reveals that <i>miR-106b-5p</i> promotes malignant phenotypes in GC by targeting retinoblastoma-like protein 2 (<i>RBL2</i>). Using <i>miR-106b-5p</i> mimic/inhibitor and <i>RBL2</i> overexpression plasmids in AGS/HGC-27 cells, this study demonstrates that <i>miR-106b-5p</i> promotes proliferation (CCK-8/clone formation) and migration/invasion (Transwell assay) and suppresses apoptosis (flow cytometry), while <i>RBL2</i> rescues these effects. Luciferase assays confirm that <i>miR-106b-5p</i> directly binds the 3’UTR of <i>RBL2</i> and western blotting demonstrates the presence of <i>RBL2</i> downregulation. Animal studies further validate the tumour-promoting role of <i>miR-106b-5p</i> via <i>RBL2</i> suppression, which suggests its therapeutic potential.</p>

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MiR-106b-5p promotes gastric cancer progression by directly targeting the tumor suppressor RBL2

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月29日

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  • Chen Luo,
  • Chunyan Wang,
  • Tonghan Chang,
  • Yuqing Niu,
  • Huanhu Zhang,
  • Feng Li,
  • Biyun Zhang

摘要

Gastric cancer (GC) is the fifth most common malignancy and the fifth highest cause of cancer-related deaths on a global scale. This study reveals that miR-106b-5p promotes malignant phenotypes in GC by targeting retinoblastoma-like protein 2 (RBL2). Using miR-106b-5p mimic/inhibitor and RBL2 overexpression plasmids in AGS/HGC-27 cells, this study demonstrates that miR-106b-5p promotes proliferation (CCK-8/clone formation) and migration/invasion (Transwell assay) and suppresses apoptosis (flow cytometry), while RBL2 rescues these effects. Luciferase assays confirm that miR-106b-5p directly binds the 3’UTR of RBL2 and western blotting demonstrates the presence of RBL2 downregulation. Animal studies further validate the tumour-promoting role of miR-106b-5p via RBL2 suppression, which suggests its therapeutic potential.