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Expression cDNA cloning of fibroblast growth factor (FGF) receptor in mouse breast cancer cells: a variant form in

H Kouhara1, S Kasayama, H Saito

  • 1Third Department of Internal Medicine, Osaka University Hospital, Japan.

Biochemical and Biophysical Research Communications
|April 15, 1991
PubMed

Insights

Researchers identified a unique fibroblast growth factor receptor (FGF-R) in mouse breast cancer cells. This altered FGF-R showed increased binding affinity for basic FGF (bFGF), suggesting a role in cancer progression.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • Fibroblast Growth Factor Receptors (FGF-Rs) play crucial roles in cell growth and differentiation.
  • Aberrant FGF-R signaling is implicated in various cancers, including breast cancer.
  • Understanding specific FGF-R alterations in cancer cells is vital for targeted therapies.

Purpose of the Study:

  • To characterize the fibroblast growth factor receptor (FGF-R) expressed in fibroblast growth factor (FGF)-responsive mouse breast cancer cells (SC-3).
  • To investigate structural differences between SC-3 cell FGF-R and normal mouse brain FGF-R.
  • To assess the functional impact of identified FGF-R variations on basic FGF (bFGF) binding.

Main Methods:

  • Construction and screening of an expression cDNA library from SC-3 mouse breast cancer cells.
  • Isolation and sequence analysis of positive FGF-R clones.
  • Site-directed mutagenesis and transfection into Chinese Hamster Ovary (CHO) cells.
  • Measurement of basic FGF (bFGF) binding affinity.

Main Results:

  • Two identical positive clones encoding a full open reading frame for FGF-R were isolated from the SC-3 cell library.
  • The SC-3 cell FGF-R exhibited a unique 12-amino acid insertion near the N-terminal region, rich in hydrophobic amino acids.
  • Additional alterations included a two-amino acid deletion in the extracellular domain and a single amino acid substitution in the C-terminal region compared to mouse brain FGF-R.
  • Transfection of the SC-3 FGF-R clone into CHO cells resulted in a significant increase in bFGF binding.

Conclusions:

  • Mouse breast cancer cells (SC-3) express a structurally distinct fibroblast growth factor receptor (FGF-R).
  • The identified modifications, particularly the N-terminal insertion, likely contribute to the enhanced binding of basic FGF (bFGF).
  • This altered FGF-R may play a role in the aberrant signaling pathways driving breast cancer progression.

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