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Updated: Jan 13, 2026

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Finding an Achilles' heel of cancer cells: Exonized Alu elements in AURKA

Beatrice Zhang1, Omar Abdel-Wahab2

  • 1Tri-Institutional Program in Computational Biology and Medicine, Weill Cornell Medicine, New York, NY, USA; Molecular Pharmacology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY, USA.

Molecular Cell
|January 9, 2026
PubMed

Insights

Researchers discovered a new mechanism driving pancreatic ductal adenocarcinoma (PDAC) through splicing factor SRSF1. This involves regulation of an Alu-derived exon in Aurora kinase A (AURKA), offering a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Regulation

Background:

  • Pancreatic ductal adenocarcinoma (PDAC) is a deadly cancer with limited therapeutic options.
  • Aberrant gene expression and splicing are hallmarks of cancer development.
  • Aurora kinase A (AURKA) is frequently overexpressed in PDAC and promotes tumorigenesis.

Purpose of the Study:

  • To identify novel mechanisms driving PDAC tumorigenesis.
  • To investigate the role of splicing factor SRSF1 in PDAC.
  • To explore the regulation of AURKA by splicing in PDAC.

Main Methods:

  • Analysis of patient-derived PDAC samples.
  • Splicing assays to study exon inclusion.
  • CRISPR-based screening to identify key splicing factors.
  • Western blotting and immunohistochemistry to assess protein levels.

Main Results:

  • SRSF1 directly regulates the inclusion of an Alu-derived exon in AURKA mRNA.
  • This aberrant splicing event leads to increased AURKA protein levels in PDAC.
  • SRSF1-mediated AURKA regulation is a critical driver of PDAC cell proliferation and survival.
  • Targeting SRSF1 or the aberrant splicing event shows therapeutic potential in preclinical models.

Conclusions:

  • SRSF1-mediated splicing of an Alu-derived exon in AURKA represents a novel mechanism of PDAC tumorigenesis.
  • This pathway is a potential target for novel PDAC therapies.
  • Further investigation into splicing-based therapeutic strategies for PDAC is warranted.

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