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Inducible nitric oxide, synthase in renal cell carcinoma: expression in tumor thrombi and induction under hypoxic

Noboru Hara1, Vladimir Bilim, Takashi Kasahara

  • 1Division of Molecular Oncology, Department of Signal Transduction Research, Niigata University Graduate School of Medical and Dental Science, Asahimachi 1, Niigata 951, Japan.

Anticancer Research
|February 26, 2004
PubMed
Abstract

Insights

Inducible nitric oxide synthase (iNOS) is linked to tumor thrombi formation in renal cell carcinoma (RCC), potentially impacting patient survival. This suggests iNOS plays a role in RCC

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Nitric oxide (NO) exhibits dual roles in carcinogenesis, acting as both an antitumor and tumor-promoting agent.
  • The specific role and expression of Nitric Oxide Synthase (NOS) in renal cell carcinoma (RCC) remain incompletely understood.

Purpose of the Study:

  • To investigate the expression and induction of inducible NOS (iNOS) in renal cell carcinoma (RCC) specimens and cell lines.
  • To elucidate the potential role of iNOS in RCC progression, particularly in relation to tumor thrombi formation and hypoxic adaptation.

Main Methods:

  • Examined iNOS expression in primary RCC lesions, metastatic sites, and tumor thrombi.
  • Assessed iNOS induction in A498 and A704 RCC cell lines under hypoxic conditions.
  • Correlated iNOS expression in tumor thrombi with cause-specific survival rates.

Main Results:

  • iNOS expression was detected in 6 out of 11 tumor thrombi, but not in primary lesions or metastatic sites.
  • Patients with iNOS-positive tumor thrombi exhibited a trend towards lower cause-specific survival rates (borderline significance).
  • Hypoxic conditions induced iNOS mRNA and protein expression in A498 and A704 RCC cells.

Conclusions:

  • Inducible NOS (iNOS) is implicated as a significant factor in RCC's ability to adapt to hypoxia.
  • iNOS expression in tumor thrombi suggests a role in venous invasion and the formation of these structures.
  • These findings highlight iNOS as a potential therapeutic target for managing advanced RCC.

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