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Interferon-gamma-induced nitric oxide inhibits the proliferation of murine renal cell carcinoma cells. | LitMetric

AI Article Synopsis

  • Renal cell carcinoma (RCC) is highly resistant to traditional treatments like chemotherapy and immunotherapy, and its low response rates may be due to the tumor's escape strategies.
  • Targeted therapies have improved patient outcomes, primarily by increasing the Th1-cytokine response (specifically IFNγ), which is important for slowing tumor growth.
  • This study found that IFNγ inhibits the growth of certain RCC cell lines by altering L-arginine metabolism and promoting nitric oxide production, suggesting potential pathways for developing new combination therapies against RCC.

Article Abstract

Renal cell carcinoma (RCC) remains one of the most resistant tumors to systemic chemotherapy, radiotherapy, and immunotherapy. Despite great progress in understanding the basic biology of RCC, the rate of responses in animal models and clinical trials using interferons (IFNs) has not improved significantly. It is likely that the lack of responses can be due to the tumor's ability to develop tumor escape strategies. Currently, the use of targeted therapies has improved the clinical outcomes of patients with RCC and is associated with an increase of Th1-cytokine responses (IFNγ), indicating the importance of IFNγ in inhibiting tumor proliferation. Thus, the present study was designed to investigate a new mechanism by which IFNγ mediates direct anti-proliferative effects against murine renal cell carcinoma cell lines. When cultured RCC cell lines were exposed to murine recombinant IFNγ, a dose dependent growth inhibition in CL-2 and CL-19 cells was observed; this effect was not observed in Renca cells. Growth inhibition in CL-2 and CL-19 cell lines was associated with the intracellular induction of nitric oxide synthase (iNOS) protein, resulting in a sustained elevation of nitric oxide (NO) and citrulline, and a decrease in arginase activity. The inhibition of cell proliferation appears to be due to an arrest in the cell cycle. The results indicate that in certain RCC cell lines, IFNγ modulates L-arginine metabolism by shifting from arginase to iNOS activity, thereby developing a potent inhibitory mechanism to encumber tumor cell proliferation and survival. Elucidating the cellular events triggered by IFNγ in murine RCC cell lines will permit anti-tumor effects to be exploited in the development of new combination therapies that interfere with L-arginine metabolism to effectively combat RCC in patients.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3445049PMC
http://dx.doi.org/10.7150/ijbs.4694DOI Listing

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