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Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells
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SRSF9 Forms Phase-Separated Condensates to Promote Ovarian Cancer Progression by Inducing RNA Alternative Splicing

Xinzhao Zuo1,2, Jie Xu1,2, Dan Yang1,2

  • 1Department of Obstetrics and Gynecology, The Third Affiliated Hospital of Chongqing Medical University, Chongqing, China.

Cancer Research
|August 7, 2025
PubMed

Insights

Serine/arginine-rich splicing factor 9 (SRSF9) drives ovarian cancer by altering NUMB mRNA splicing. Targeting SRSF9 or NUMB mRNA splicing inhibits tumor growth, offering new therapeutic strategies for ovarian cancer.

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • RNA Biology

Background:

  • Deregulation of RNA alternative splicing and modification is crucial in cancer development.
  • Understanding the interplay between RNA splicing and modifications offers insights into cancer biology.

Purpose of the Study:

  • To investigate the role of serine/arginine-rich splicing factor 9 (SRSF9) in ovarian cancer (OC).
  • To elucidate the mechanism by which SRSF9 influences NUMB mRNA splicing and its impact on OC progression.

Main Methods:

  • Investigated SRSF9's recognition of non-N6-methyladenosine (m6A)-modified NUMB mRNA.
  • Analyzed SRSF9-mediated alternative splicing and its antagonism by NUMB mRNA m6A modification.
  • Studied the role of SRSF9 nuclear condensates in splicing and tumor promotion.
  • Assessed SRSF9 expression levels and their correlation with OC patient prognosis.
  • Evaluated the effects of SRSF9 loss or NUMB mRNA isoform switch inhibition on OC growth in vitro and in vivo.

Main Results:

  • SRSF9 recognizes non-m6A-modified NUMB mRNA, inducing an oncogenic isoform switch in OC.
  • NUMB mRNA m6A modification counteracts SRSF9-driven alternative splicing.
  • SRSF9 forms nuclear condensates essential for its splicing function and tumor-promoting activity in OC.
  • SRSF9 is upregulated in OC and associated with poor patient prognosis.
  • Inhibiting SRSF9 or inducing a NUMB mRNA isoform switch suppressed OC growth.

Conclusions:

  • SRSF9 condensation promotes OC progression by modulating alternative splicing in competition with m6A modification.
  • SRSF9 represents a potential therapeutic target for ovarian cancer.

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