<p>SNRPB2, a spliceosome component, is well known to participate in the pre-splicing of mRNA and enhance the apoptosis induction impact of ixazomib on multiple myeloma cells. However, its precise effect on hepatocellular carcinoma (HCC) remains unexplored. Here, we demonstrate that high level of SNRPB2 is significantly associated with poor outcomes in HCC patients. Additionally, inhibiting SNRPB2 may accelerate ferroptosis, thereby suppressing HCC tumor development. Moreover, SNRPB2 is regulated by the SNHG4/miR-204-5p axis, and increased SNHG4 could reverse the effect of SNRPB2 knockdown. Finally, SNRPB2 deficiency increases the sorafenib sensitivity of HCC cells. Conclusively, our study uncovers the previously unknown role of SNRPB2 in HCC, reveals the related ceRNA regulatory axis of SNRPB2, and identifies a novel ferroptosis regulating protein, suggesting SNRPB2 appears to be a promising target for HCC therapy.</p>

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Small nuclear ribonucleoprotein polypeptide B2 regulated by SNHG4/miR-204-5p axis inhibits ferroptosis to aggravate the progression of hepatocellular carcinoma

  • Jiaxing Guo,
  • Lingshu Li,
  • Haiyan Wang,
  • Zhenqin Gao,
  • Chanjuan Shen,
  • Bokang Yan

摘要

SNRPB2, a spliceosome component, is well known to participate in the pre-splicing of mRNA and enhance the apoptosis induction impact of ixazomib on multiple myeloma cells. However, its precise effect on hepatocellular carcinoma (HCC) remains unexplored. Here, we demonstrate that high level of SNRPB2 is significantly associated with poor outcomes in HCC patients. Additionally, inhibiting SNRPB2 may accelerate ferroptosis, thereby suppressing HCC tumor development. Moreover, SNRPB2 is regulated by the SNHG4/miR-204-5p axis, and increased SNHG4 could reverse the effect of SNRPB2 knockdown. Finally, SNRPB2 deficiency increases the sorafenib sensitivity of HCC cells. Conclusively, our study uncovers the previously unknown role of SNRPB2 in HCC, reveals the related ceRNA regulatory axis of SNRPB2, and identifies a novel ferroptosis regulating protein, suggesting SNRPB2 appears to be a promising target for HCC therapy.