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Updated: Jan 21, 2026

A Syngeneic Mouse Model of Metastatic Renal Cell Carcinoma for Quantitative and Longitudinal Assessment of Preclinical Therapies
Published on: April 12, 2017
Glutathione Metabolism in Renal Cell Carcinoma Progression and Implications for Therapies
Yi Xiao1,2, David Meierhofer3
1Max Planck Institute for Molecular Genetics, Ihnestraße 63-73, 14195 Berlin, Germany.
Abstract:
A significantly increased level of the reactive oxygen species (ROS) scavenger glutathione (GSH) has been identified as a hallmark of renal cell carcinoma (RCC). The proposed mechanism for increased GSH levels is to counteract damaging ROS to sustain the viability and growth of the malignancy. Here, we review the current knowledge about the three main RCC subtypes, namely clear cell RCC (ccRCC), papillary RCC (pRCC), and chromophobe RCC (chRCC), at the genetic, transcript, protein, and metabolite level and highlight their mutual influence on GSH metabolism. A further discussion addresses the question of how the manipulation of GSH levels can be exploited as a potential treatment strategy for RCC.
Insights
Renal cell carcinoma (RCC) exhibits elevated glutathione (GSH), a reactive oxygen species (ROS) scavenger. Targeting GSH metabolism presents a promising therapeutic strategy for RCC treatment.
Area of Science:
- Oncology
- Biochemistry
- Metabolism
Background:
- Elevated glutathione (GSH) levels are a hallmark of renal cell carcinoma (RCC), crucial for malignancy survival.
- Increased GSH counteracts reactive oxygen species (ROS), supporting cancer cell viability and growth.
Purpose of the Study:
- To review current knowledge on three main RCC subtypes (ccRCC, pRCC, chRCC).
- To highlight the influence of RCC subtypes on GSH metabolism.
- To discuss GSH manipulation as a potential RCC treatment strategy.
Main Methods:
- Literature review of genetic, transcriptomic, proteomic, and metabolomic data for RCC subtypes.
- Analysis of the interplay between RCC subtypes and GSH metabolism.
- Discussion of therapeutic strategies targeting GSH.
Main Results:
- RCC subtypes (ccRCC, pRCC, chRCC) exhibit distinct molecular profiles.
- GSH metabolism is significantly altered across RCC subtypes.
- Interactions between cancer genetics and GSH pathways are evident.
Conclusions:
- Understanding subtype-specific GSH alterations is key.
- Targeting GSH metabolism offers a potential therapeutic avenue for RCC.
- Further research into GSH-modulating agents is warranted for RCC treatment.
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