FGFR3 mutation affects cell growth, apoptosis and attachment in keratinocytes

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Updated: Jun 13, 2026

Characterization of In Vitro Differentiation of Human Primary Keratinocytes by RNA-Seq Analysis
07:29

Characterization of In Vitro Differentiation of Human Primary Keratinocytes by RNA-Seq Analysis

Published on: May 16, 2020

Christian Hafner1, Erica Di Martino, Eva Pitt

  • 1Department of Dermatology, University of Regensburg, Regensburg, Germany. christian.hafner@klinik.uni-regensburg.de

Experimental Cell Research
|April 28, 2010
PubMed

Insights

Fibroblast growth factor receptor 3 (FGFR3) mutations increase cell number and decrease apoptosis in skin cells. This may contribute to the development of benign skin tumors like seborrheic keratosis.

Area of Science:

  • Dermatology
  • Molecular Biology
  • Oncology

Background:

  • Fibroblast growth factor receptor 3 (FGFR3) mutations are found in benign skin lesions.
  • The functional impact of these FGFR3 mutations in human skin remains unclear.

Purpose of the Study:

  • To investigate the functional effects of the common R248C FGFR3 mutation in human keratinocytes.
  • To understand the cellular mechanisms underlying FGFR3-driven benign skin tumor development.

Main Methods:

  • Stable transduction of HaCaT keratinocytes with wildtype or R248C FGFR3 IIIb cDNA.
  • Analysis of cell growth, apoptosis, attachment, migration, and senescence.
  • Microarray analysis and Western blotting for ERK1/2 phosphorylation.

Main Results:

  • FGFR3 mutant keratinocytes showed increased cell numbers at confluence compared to wildtype.
  • Mutant cells exhibited significantly lower apoptosis and decreased fibronectin attachment.
  • Enhanced ERK1/2 phosphorylation was observed in confluent FGFR3 mutant cells.

Conclusions:

  • Increased cell proliferation and reduced apoptosis due to FGFR3 mutations may drive acanthotic tumor formation in the skin.
  • The R248C FGFR3 mutation influences keratinocyte behavior, potentially contributing to benign skin lesion pathogenesis.

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