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Cellular retinoic acid binding protein I: expression and functional influence in renal cell carcinoma

Susanne Pfoertner1, Ulrike Goelden, Wiebke Hansen

  • 1Department of Cell Biology and Immunology, German Research Center for Biotechnology, Braunschweig, Germany.

Tumour Biology : the Journal of the International Society for Oncodevelopmental Biology and Medicine
|October 29, 2005
PubMed

Insights

Retinoic acid (RA) shows anti-cancer effects, but its use in metastatic renal cell carcinoma (RCC) is limited. This study found CRABP-I is underexpressed in RCC, and its presence confers resistance to RA treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Retinoic acid (RA) exhibits anti-proliferative and tumor-suppressive properties.
  • The efficacy of RA in metastatic renal cell carcinoma (RCC) treatment has been suboptimal.
  • The precise mechanisms of RA action and the role of cellular RA binding proteins (CRABP) in RCC remain unclear.

Purpose of the Study:

  • To investigate the expression of cellular retinoic acid binding protein-I (CRABP-I) in RCC.
  • To determine the influence of CRABP-I on the response to RA in RCC.
  • To elucidate the molecular mechanisms underlying RA and CRABP-I interactions in RCC.

Main Methods:

  • Real-time RT-PCR was used to analyze CRABP-I expression in RCC cell lines and primary samples.
  • CRABP-I was stably transfected into A-498 RCC cells to create a cellular model.
  • Gene expression profiling was performed using a human CodeLink UniSet Bioarray to compare CRABP-I-expressing cells with controls.

Main Results:

  • CRABP-I expression was significantly lower in RCC cell lines and primary tumors compared to adjacent normal kidney tissue.
  • CRABP-I-transfected RCC cells demonstrated resistance to all-trans retinoic acid (ATRA) and 9-cis RA.
  • Gene expression analysis revealed specific regulation of 54 genes in CRABP-I-expressing cells, impacting transcriptional control, signaling, apoptosis, cell cycle, and metabolism.

Conclusions:

  • CRABP-I is underexpressed in renal cell carcinoma.
  • CRABP-I expression confers resistance to retinoic acid treatment in RCC cells.
  • These findings enhance understanding of RA's role in RCC and CRABP-I-mediated signaling pathways.

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