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<p>This study explores the mechanism of miR-19b-3p in bladder cancer (BCa) cell proliferation and apoptosis to provide the latest theoretical basis for miR-19b-3p to become a novel biomarker and therapeutic target for BCa. miR-19b-3p, lncRNA SNHG20, and HS3ST3B1 expressions in BCa tissues or cells were detected via RT-qPCR or Western blot. Cell proliferation was evaluated via CCK-8 and colony formation assays. Cell apoptosis was assessed via flow cytometry, and apoptosis related factors Bax and Bcl-2 were detected via Western blot. Dual luciferase and RIP assays confirmed the binding of miR-19b-3p and lncRNA SNHG20. The binding between lncRNA SNHG20, TARDBP, and HS3ST3B1 was analyzed by RIP, RNA pull down, and co-immunoprecipitation. The RNA stability of lncRNA SNHG20 and HS3ST3B1 was tested after actinomycin D treatment. A nude mouse xenograft tumor model was established to validate the effect of miR-19b-3p on BCa in vivo. miR-19b-3p was weakly expressed in BCa, while lncRNA SNHG20 and HS3ST3B1 were highly expressed. Overexpression of miR-19b-3p repressed BCa cell proliferation but facilitated apoptosis. Mechanistically, miR-19b-3p decreased lncRNA SNHG20 expression by binding to lncRNA SNHG20 and reducing its stability, thus repressing the interaction between lncRNA SNHG20-TARDBP-HS3ST3B1. Further in vivo experiments also revealed that miR-19b-3p restrained the in vivo tumorigenicity of BCa cells and promoted apoptosis by suppressing the lncRNA SNHG20/HS3ST3B1 axis. In conclusion, overexpression of miR-19b-3p represses BCa cell proliferation and promotes apoptosis by suppressing the lncRNA SNHG20/HS3ST3B1 axis.</p>

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miR-19b-3p Affects the Proliferation and Apoptosis of Bladder Cancer Cells by Regulating the Stability of lncRNA SNHG20

  • 期刊论文

  • 发表日期：

    2025年9月6日

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  • Hongshuang Dai,
  • Yunzhu Zhang,
  • Siwen Yu,
  • Yue Feng,
  • Zhongjie Qiao

摘要

This study explores the mechanism of miR-19b-3p in bladder cancer (BCa) cell proliferation and apoptosis to provide the latest theoretical basis for miR-19b-3p to become a novel biomarker and therapeutic target for BCa. miR-19b-3p, lncRNA SNHG20, and HS3ST3B1 expressions in BCa tissues or cells were detected via RT-qPCR or Western blot. Cell proliferation was evaluated via CCK-8 and colony formation assays. Cell apoptosis was assessed via flow cytometry, and apoptosis related factors Bax and Bcl-2 were detected via Western blot. Dual luciferase and RIP assays confirmed the binding of miR-19b-3p and lncRNA SNHG20. The binding between lncRNA SNHG20, TARDBP, and HS3ST3B1 was analyzed by RIP, RNA pull down, and co-immunoprecipitation. The RNA stability of lncRNA SNHG20 and HS3ST3B1 was tested after actinomycin D treatment. A nude mouse xenograft tumor model was established to validate the effect of miR-19b-3p on BCa in vivo. miR-19b-3p was weakly expressed in BCa, while lncRNA SNHG20 and HS3ST3B1 were highly expressed. Overexpression of miR-19b-3p repressed BCa cell proliferation but facilitated apoptosis. Mechanistically, miR-19b-3p decreased lncRNA SNHG20 expression by binding to lncRNA SNHG20 and reducing its stability, thus repressing the interaction between lncRNA SNHG20-TARDBP-HS3ST3B1. Further in vivo experiments also revealed that miR-19b-3p restrained the in vivo tumorigenicity of BCa cells and promoted apoptosis by suppressing the lncRNA SNHG20/HS3ST3B1 axis. In conclusion, overexpression of miR-19b-3p represses BCa cell proliferation and promotes apoptosis by suppressing the lncRNA SNHG20/HS3ST3B1 axis.