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Transformation by oncogenic ras-p21 alters the processing and subcellular localization of the lysosomal protease

M Démoz1, R Castino, A Dragonetti

  • 1Department of Medical Sciences, A. Avogadro University, Novara, Italy.

Insights

Ras oncogene transformation alters cathepsin D (CD) processing and localization in fibroblasts. These changes suggest ras GTPase critically regulates transport between post-Golgi organelles.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • Cathepsin D (CD) is an endosomal-lysosomal protease implicated in cancer progression.
  • The c-Ha-ras oncogene plays a role in cell signaling and transformation.

Purpose of the Study:

  • To investigate the impact of ras oncogene transformation on cathepsin D expression, processing, and intracellular localization.
  • To elucidate the role of ras GTPase in regulating post-Golgi organelle transport.

Main Methods:

  • Analysis of cathepsin D molecular forms in ras-transfected and parental rat embryo fibroblasts.
  • Treatment with ammonium chloride to assess pH-dependent processing.
  • Microscopic examination of cathepsin D localization in different cell types.
  • Evaluation of serum deprivation effects on cell growth and CD activity.

Main Results:

  • Ras transformation altered the pattern of mature cathepsin D molecular forms, with reduced 45 kDa and absent 30+14 kDa species.
  • Ammonium chloride induced accumulation of specific mature CD forms in both cell types but with distinct patterns.
  • Ras-transformed cells showed fewer, peripherally located CD-positive vacuoles compared to perinuclear distribution in controls.
  • Serum deprivation did not affect ras-transformed cell growth or CD accumulation, unlike control cells.

Conclusions:

  • Ras oncogene significantly alters cathepsin D processing and intracellular trafficking.
  • Ras GTPase appears to be a key regulator of transport dynamics within post-Golgi compartments.
  • These findings highlight a potential role for CD dysregulation in ras-mediated oncogenesis.

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