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Related Experiment Video

Updated: Dec 20, 2025

Studying Pancreatic Cancer Stem Cell Characteristics for Developing New Treatment Strategies
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An FGFR/AKT/SOX2 Signaling Axis Controls Pancreatic Cancer Stemness.

Mei-Yu Quan1, Qiang Guo1, Jiayu Liu2

  • 1School of Pharmaceutical Sciences and International Collaborative Center on Growth Factor Research, Wenzhou Medical University, Wenzhou, China.

Frontiers in Cell and Developmental Biology
|May 28, 2020
PubMed
Summary
This summary is machine-generated.

Fibroblast growth factor receptor (FGFR) signaling drives cancer stemness in pancreatic ductal adenocarcinoma. Inhibiting FGFR, AKT, or SOX2 may offer new therapeutic strategies for this aggressive cancer.

Keywords:
FGFRSOX2pancreatic cancersphere-formation assaystemness

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Cancer stemness, characterized by high malignancy and therapeutic resistance, is a hallmark of aggressive tumors like pancreatic ductal adenocarcinoma (PDAC).
  • Fibroblast growth factors (FGFs) and their receptors (FGFRs) are implicated in maintaining stem cell pluripotency and cancer stemness, but their precise role in PDAC remains unclear.
  • FGF signaling is a key component of media used to culture cancer stemness-inducing (CSI) cells and organoids.

Purpose of the Study:

  • To elucidate the role of FGF/FGFR signaling in maintaining cancer stemness in pancreatic ductal adenocarcinoma.
  • To identify the molecular mechanisms by which FGFR signaling influences PDAC stemness.
  • To evaluate the therapeutic potential of targeting the FGFR pathway in PDAC.

Main Methods:

  • Inhibition of FGF/FGFR signaling in PDAC cells in vitro and in vivo.
  • Knockdown of FGFR1 and FGFR2 expression.
  • Assessment of sphere-forming ability and tumorigenesis.
  • Analysis of SOX2 expression and localization.
  • Investigation of AKT phosphorylation and activity.
  • Pharmacological inhibition of AKT in CSI medium.

Main Results:

  • Inhibition of FGF/FGFR signaling reduced sphere formation in PDAC cells in vitro.
  • Knockdown of FGFR1 and FGFR2 diminished PDAC tumorigenesis in vivo.
  • FGFR signaling loss led to SOX2 downregulation; SOX2 overexpression induced spheroid formation.
  • FGFR inhibition reduced AKT phosphorylation; AKT inhibition in CSI medium caused loss of spheroid formation, SOX2 nuclear expression, and increased SOX2 degradation.

Conclusions:

  • An FGFR/AKT/SOX2 signaling axis is identified as a critical regulator of cancer stemness in PDAC.
  • This axis represents a potential therapeutic target for combating PDAC, an aggressive malignancy.
  • Targeting FGFR, AKT, or SOX2 may be a viable strategy to overcome therapeutic resistance in PDAC.