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Disruption of the SNRPF-DDX24-E2F4 Feedback Loop Uncouples Splicing and Transcriptional Regulation to Suppress

Yingwei Li1, Zhongshao Chen2, Qianqian Gao2

  • 1Department of Obstetrics and Gynecology, Shandong Key Laboratory of Reproductive Health and Birth Defects Prevention and Control, Qilu Hospital of Shandong University, Medical Integration and Practice Center, Cheeloo College of Medicine, Shandong University, Ji'nan, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|May 10, 2026
PubMed

Insights

Ovarian cancer progression is driven by SNRPF, a spliceosome component. Inhibiting SNRPF disrupts a key feedback loop, reducing oncogenic drivers and impairing tumor growth, offering a new therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Ovarian cancer (OC) is a leading cause of gynecologic cancer mortality.
  • Targeted therapy for OC is limited by understanding post-transcriptional oncogenic drivers.
  • Dysregulated RNA splicing, especially intron retention (IR), is a key tumor progression driver.

Purpose of the Study:

  • Identify novel post-transcriptional oncogenic drivers in ovarian cancer.
  • Investigate the role of SNRPF in OC progression.
  • Elucidate the "SNRPF-DDX24-E2F4" axis linking splicing and transcription.

Main Methods:

  • Integrated transcriptomic and proteomic analyses.
  • SNRPF silencing and knockdown experiments.
  • Intron retention analysis, nonsense-mediated decay (NMD) assays.
  • Antisense oligonucleotide (ASO)-mediated inhibition of SNRPF.
  • In vitro, in vivo, and patient-derived xenograft models.

Main Results:

  • SNRPF is overexpressed in OC tumors and predicts poor survival.
  • SNRPF silencing suppresses OC proliferation, invasion, and xenograft growth.
  • SNRPF regulates DDX24 and E2F4 expression via IR and NMD, forming a self-sustaining axis.
  • ASO-mediated SNRPF inhibition disrupts the axis and impairs tumor growth.

Conclusions:

  • SNRPF is a potent oncogenic driver in ovarian cancer.
  • A novel splicing-transcription coupling mechanism involving SNRPF, DDX24, and E2F4 drives OC.
  • SNRPF represents a promising therapeutic target for ovarian cancer.
Keywords:
RNA splicingSNRPFintron retentionovarian cancertherapeutic targets

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