Research Paper Volume 13, Issue 1 pp 537—554

SNRPB-mediated RNA splicing drives tumor cell proliferation and stemness in hepatocellular carcinoma

Yu-Ting Zhan1, *, , Lei Li1,2, *, , Ting-Ting Zeng1, , Ning-Ning Zhou1, , Xin-Yuan Guan1,2, , Yan Li1, ,

  • 1 State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou 510060, P. R. China
  • 2 Department of Clinical Oncology, The University of Hong Kong, Hong Kong 852, P. R. China
* Equal contribution

Received: May 18, 2020       Accepted: September 28, 2020       Published: December 3, 2020
How to Cite

Copyright: © 2020 Zhan et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Hepatocellular carcinoma (HCC) is one of the leading malignant diseases worldwide, but therapeutic targets for HCC are lacking. Here, we characterized a significant upregulation of Small Nuclear Ribonucleoprotein Polypeptides B and B1 (SNRPB) in HCC via qRT-PCR, western blotting, tissue microarray and public database analyses. Increased SNRPB expression was positively associated with adjacent organ invasion, tumor size, serum AFP level and poor HCC patient survival. Next, we transfected SNRPB into HCC cells to construct SNRPB-overexpressing cell lines, and short hairpin RNA targeting SNRPB was used to silence SNRPB in HCC cells. Functional studies showed that SNRPB overexpression could promote HCC cell malignant proliferation and stemness maintenance. Inversely, SNRPB knockdown in HCC cells caused inverse effects. Importantly, analysis of alternative splicing by RNA sequencing revealed that SNRPB promoted the formation of AKT3-204 and LDHA-220 splice variants, which activated the Akt pathway and aerobic glycolysis in HCC cells. In conclusion, SNRPB could serve as a prognostic predictor for patients with HCC, and it promotes HCC progression by inducing metabolic reprogramming.


GEO: Gene Expression Omnibus; GO: Gene Ontology; HCC: hepatocellular carcinoma; IHC: immunehisto chemical; PBS: phosphate buffered saline; qRT-PCR: quantitative reverse transcription PCR; RT-PCR: reverse transcription PCR; SAPs: spliceosome-associated proteins; shRNA: short hairpin RNA; snRNPs: small nuclear ribonucleoproteins; SNRPB: Small Nuclear Ribonucle oprotein Polypeptides B and B1; TBST: Tris-buffered saline/Tween 20; TCGA: The Cancer Genome Atlas.