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Updated: Feb 1, 2026

Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells
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Splicing Factor SF3B4 Suppresses Pancreatic Cancer Growth and Migration by Inhibiting Autophagy

So-Hyun Choi1,2,3, Jiyoon Seo1,2,3, Seung Min Jeong4,2,3

  • 1Department of Biochemistry, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.

Anticancer Research
|January 30, 2026
PubMed
Abstract

Insights

SF3B4 acts as a tumor suppressor in pancreatic cancer by inhibiting autophagy and increasing reactive oxygen species (ROS). This finding offers a new strategy to combat pancreatic ductal adenocarcinoma (PDAC) and chemoresistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Metabolism

Background:

  • Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal cancer with known chemoresistance and metabolic adaptations like increased autophagy.
  • The splicing factor SF3B4's role in PDAC is not well understood, despite its oncogenic function in other cancers.

Purpose of the Study:

  • To investigate the functional and mechanistic role of SF3B4 in pancreatic ductal adenocarcinoma (PDAC).

Main Methods:

  • SF3B4 expression analysis in PDAC patient datasets and experimental models.
  • Functional assays assessing cell proliferation, colony formation, migration, and autophagy in PDAC cells.
  • Evaluation of reactive oxygen species (ROS) levels, 5-fluorouracil (5-FU) sensitivity, and apoptotic responses.

Main Results:

  • SF3B4 functions as a tumor suppressor in PDAC by inhibiting autophagy, a critical survival pathway for this cancer.
  • SF3B4 overexpression reduced PDAC cell proliferation, colony formation, and migration.
  • SF3B4 suppressed autophagic flux, leading to increased ROS, which inhibited tumor phenotypes. This effect was reversed by N-acetylcysteine (NAC).
  • SF3B4 overexpression enhanced PDAC cell sensitivity to 5-FU and increased apoptosis.

Conclusions:

  • SF3B4 acts as a context-dependent tumor suppressor in PDAC by modulating autophagy and redox homeostasis.
  • The SF3B4-autophagy-ROS pathway presents a potential therapeutic target for suppressing PDAC progression and overcoming chemoresistance.
Keywords:
PDACROSSF3B4autophagychemoresistance

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