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Absence of the CAAX endoprotease Rce1: effects on cell growth and transformation

Martin O Bergo1, Patricia Ambroziak, Cria Gregory

  • 1Gladstone Institute of Cardiovascular Disease, University of California, San Francisco, California 94141-9100, USA.

Insights

Blocking Ras endoproteolytic processing via Rce1 inhibition slows cell growth and limits cancer cell transformation. This study developed a cell system to investigate Rce1

Area of Science:

  • Biochemistry
  • Cell Biology
  • Oncology

Background:

  • Ras proteins and other CAAX proteins require post-isoprenylation processing, including endoproteolytic cleavage by Rce1 and methylation by Icmt.
  • This processing is crucial for Ras protein membrane association and is a potential target for cancer therapy.
  • Previous studies suggested inhibiting Rce1 could impede cell growth and transformation.

Purpose of the Study:

  • To establish a cell culture system for studying the effects of blocking post-isoprenylation processing.
  • To investigate the role of Rce1 in Ras protein processing, cell growth, and transformation.
  • To evaluate the therapeutic potential of Rce1 inhibition in cancer cells.

Main Methods:

  • Generation of mice with a conditional Rce1 allele (Rce1(flox)).
  • Production of Rce1(flox/flox) and Rce1(Delta/Delta) fibroblasts via Cre-mediated excision.
  • Analysis of Ras protein processing, localization, cell growth, and transformation (soft agar assay).
  • Assessment of Rce1 excision effects on skin carcinoma cell line growth, with and without farnesyltransferase inhibitor treatment.

Main Results:

  • Cre-mediated Rce1 excision in fibroblasts eliminated Ras endoproteolytic processing and methylation.
  • Truncated K-Ras and H-Ras fusion proteins showed partial mislocalization in Rce1-deficient cells.
  • Rce1(Delta/Delta) fibroblasts exhibited slower growth compared to Rce1(flox/flox) fibroblasts.
  • Rce1 excision reduced Ras-induced transformation and significantly retarded skin carcinoma cell growth.
  • Combined Rce1 inhibition and farnesyltransferase inhibitor treatment enhanced the anti-cancer effect.

Conclusions:

  • Interference with post-isoprenylation processing, specifically Rce1 activity, retards cell growth.
  • Blocking Rce1 limits Ras-induced cell transformation, offering a strategy for cancer therapy.
  • Rce1 inhibition sensitizes tumor cells to farnesyltransferase inhibitors, suggesting combination therapy potential.

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