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Updated: Feb 11, 2026

Heterotypic Three-dimensional In Vitro Modeling of Stromal-Epithelial Interactions During Ovarian Cancer Initiation and Progression
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Heterotypic Three-dimensional In Vitro Modeling of Stromal-Epithelial Interactions During Ovarian Cancer Initiation and Progression

Published on: August 28, 2012

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FGFRL1 Promotes Ovarian Cancer Progression by Crosstalk with Hedgehog Signaling

Haiyan Tai1, Zhiyong Wu1, Su'an Sun2

  • 1Obstetrics and Gynecology Hospital, Fudan University, Shanghai 200011, China.

Journal of Immunology Research
|April 21, 2018
PubMed

Insights

Fibroblast growth factor receptor-like-1 (FGFRL1) is upregulated in ovarian carcinoma (OC), promoting tumor growth and progression. Targeting FGFRL1 and its associated Hedgehog signaling pathways may offer new therapeutic strategies for OC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Fibroblast growth factor receptor-like-1 (FGFRL1), the fifth fibroblast growth factor receptor, has largely uncharacterized biological functions, especially in cancer.
  • Understanding FGFRL1's role is crucial for advancing ovarian carcinoma (OC) research and treatment.

Purpose of the Study:

  • To investigate the expression profile and biological functions of FGFRL1 in ovarian carcinoma (OC).
  • To explore the underlying mechanisms of FGFRL1 regulation and its impact on tumor progression.

Main Methods:

  • Gene expression analysis using arrays and databases.
  • In vitro assays (proliferation, apoptosis, migration) and in vivo xenograft models.
  • Chromatin immunoprecipitation PCR and microarray hybridization to elucidate molecular mechanisms.

Main Results:

  • FGFRL1 was significantly upregulated in OC tissues and correlated with poor prognosis.
  • FGFRL1 knockdown inhibited OC cell proliferation, migration, and in vivo tumor growth.
  • Hypoxia induces FGFRL1 via hypoxia-inducible factor 1α, and FGFRL1 crosstalks with Hedgehog signaling.

Conclusions:

  • FGFRL1 is a potential prognostic biomarker for OC.
  • FGFRL1 plays a critical role in OC progression through hypoxia-inducible factor 1α and Hedgehog signaling.
  • FGFRL1 and associated pathways represent potential therapeutic targets for OC treatment.

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