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The Use of Reverse Phase Protein Arrays (RPPA) to Explore Protein Expression Variation within Individual Renal Cell Cancers
12:22

The Use of Reverse Phase Protein Arrays (RPPA) to Explore Protein Expression Variation within Individual Renal Cell Cancers

Published on: January 22, 2013

Expression and functional influence of cellular retinoic acid-binding protein II in renal cell carcinoma

Ulrike Goelden1, Susanne Pfoertner, Wiebke Hansen

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

Urologia Internationalis
|October 11, 2005
PubMed
Abstract

Insights

Retinoic acid (RA) shows promise in cancer treatment, but its effectiveness in renal cell carcinoma (RCC) is limited. This study found CRABP-II is downregulated in RCC tumors, and its overexpression did not significantly alter RA

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Retinoic acid (RA) derivatives have demonstrated antiproliferative and tumor-suppressive properties, utilized in treating various cancers.
  • The efficacy of RA in metastatic renal cell carcinoma (RCC) has not met initial expectations, necessitating further investigation into its mechanisms.
  • The precise roles of RA action and cellular retinoic acid-binding proteins (CRABP) in RCC remain unclear.

Purpose of the Study:

  • To investigate the expression of cellular retinoic acid-binding protein II (CRABP-II) in renal cell carcinoma (RCC).
  • To evaluate the potential influence of CRABP-II on the response to retinoic acid (RA) in RCC.
  • To explore the relationship between CRABP-II expression levels and RA-induced antiproliferative effects in RCC cells.

Main Methods:

  • Real-time RT-PCR was employed to assess CRABP-II expression in 12 RCC samples and adjacent normal kidney tissues.
  • CRABP-II was cloned and overexpressed in the CAKI-2 RCC cell line.
  • Antiproliferative effects of all-trans RA (ATRA) and 9-cis RA were evaluated in CRABP-II (un)transfected CAKI-2 cells using 3H-thymidine-proliferation assays.

Main Results:

  • CRABP-II expression was found to be downregulated in primary RCC tumor samples compared to corresponding normal kidney tissue (median tumor/kidney ratios of 0.16 and 0.12).
  • Overexpression of CRABP-II in CAKI-2 RCC cells did not lead to a significant change in sensitivity to RA.
  • CRABP-II overexpressing cells appeared less sensitive to RA stimulation than cells with naturally low CRABP-II levels.

Conclusions:

  • CRABP-II expression is downregulated in primary RCC tumors relative to normal kidney tissue.
  • Overexpression of CRABP-II in RCC cells did not significantly impact RA-mediated antiproliferative effects.
  • Further research is required to elucidate the exact function of CRABP-II and its downregulation in RCC, including its interactions within the RA signaling pathway.

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