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Updated: Oct 5, 2026

Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes
15:43

Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes

Published on: January 7, 2013

Constitutive activation of nuclear factor-kappaB prevents TRAIL-induced apoptosis in renal cancer cells

M Oya1, M Ohtsubo, A Takayanagi

  • 1Department of Urology, Keio University School of Medicine, Shinjuku-ku, Tokyo 160-8582, Japan. moto-oya@med.keio.ac.jp

Oncogene
|July 6, 2001
PubMed

Insights

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) resistance in renal cell carcinoma is linked to NF-kappaB activation. Targeting NF-kappaB may offer a promising therapy for resistant cancer cells.

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • TRAIL induces apoptosis in cancer cells via death receptors.
  • Some cancer cells exhibit TRAIL resistance despite receptor expression.
  • An inhibitory factor is implicated in TRAIL resistance.

Purpose of the Study:

  • Investigate the mechanism of TRAIL resistance in renal cell carcinoma (RCC).
  • Identify key molecular players in TRAIL-resistant RCC.
  • Explore therapeutic strategies for TRAIL-resistant RCC.

Main Methods:

  • Assessed NF-kappaB activity in TRAIL-sensitive and resistant RCC cell lines.
  • Manipulated IkappaBalpha expression (inhibitor of NF-kappaB) in RCC cells.
  • Utilized antisense cDNA and adenoviral vectors for gene expression.

Main Results:

  • Constitutive NF-kappaB activation was observed in TRAIL-resistant RCC cell lines.
  • Inhibition of NF-kappaB (via IkappaBalpha expression) restored TRAIL sensitivity.
  • Forced NF-kappaB activation induced TRAIL resistance in sensitive cells.

Conclusions:

  • NF-kappaB is a critical factor in TRAIL resistance in RCC.
  • RCC can be categorized into TRAIL-sensitive (low NF-kappaB) and TRAIL-resistant (high NF-kappaB) subsets.
  • TRAIL is a potential treatment for sensitive RCC, while NF-kappaB targeted therapies are promising for resistant RCC.

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