Guo Jiaxing, Li Lingshu, Wang Haiyan, Gao Zhenqin, Shen Chanjuan, Yan Bokang
Department of Hematology, Zhuzhou Hospital Affiliated to Xiangya School of Medicine, Central South University, Zhuzhou, 412007, Hunan, China.
Academy of Biomedical Engineering, Kunming Medical University, Kunming, 650500, Yunnan, China.
Discov Oncol. 2025 Jul 16;16(1):1349. doi: 10.1007/s12672-025-03192-w.
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.
剪接体成分SNRPB2众所周知参与mRNA的前体剪接,并增强伊沙佐米对多发性骨髓瘤细胞的凋亡诱导作用。然而,其对肝细胞癌(HCC)的确切作用仍未被探索。在此,我们证明高水平的SNRPB2与HCC患者的不良预后显著相关。此外,抑制SNRPB2可能加速铁死亡,从而抑制HCC肿瘤发展。而且,SNRPB2受SNHG4/miR-204-5p轴调控,SNHG4增加可逆转SNRPB2敲低的作用。最后,SNRPB2缺陷增加HCC细胞对索拉非尼的敏感性。总之,我们的研究揭示了SNRPB2在HCC中先前未知的作用,揭示了SNRPB2相关的ceRNA调控轴,并鉴定出一种新型铁死亡调节蛋白,表明SNRPB2似乎是HCC治疗的一个有前景的靶点。