ArticleCell cycle (Georgetown, Tex.)2010
Increasing reactive oxygen species as a therapeutic approach to treat hereditary leiomyomatosis and renal cell carcinoma.
Article in Cell cycle (Georgetown, Tex.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Metabolism of kidney cancer: from the lab to clinical practice.European urology · 2013Pooled it
- Targeting NAD+ Metabolism Vulnerability in FH-Deficient Hereditary Leiomyomatosis and Renal Cell Carcinoma with the Novel NAMPT Inhibitor OT-82.Molecular cancer therapeutics · 2025Article
- Knowledge-Based Therapeutics for Tricarboxylic Acid (TCA) Cycle-Deficient Cancers.Cold Spring Harbor perspectives in medicine · 2024Review
- Characterization of genetically defined sporadic and hereditary type 1 papillary renal cell carcinoma cell lines.Genes, chromosomes & cancer · 2021Article
- Advances in hereditary leiomyomatosis and renal cell carcinoma (HLRCC) research.Seminars in cancer biology · 2020Review
- Choosing The Right Animal Model for Renal Cancer Research.Translational oncology · 2020Review
- Synthetically Lethal Interactions of Heme Oxygenase-1 and Fumarate Hydratase Genes.Biomolecules · 2020Article
- Proteasome inhibition disrupts the metabolism of fumarate hydratase- deficient tumors by downregulating p62 and c-Myc.Scientific reports · 2019Article
- Role of Positron Emission Tomography Imaging in Metabolically Active Renal Cell Carcinoma.Current urology reports · 2019Review
- Metabolic Pathways in Kidney Cancer: Current Therapies and Future Directions.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2018Review
- Fumarate hydratase inactivation in hereditary leiomyomatosis and renal cell cancer is synthetic lethal with ferroptosis induction.Cancer science · 2018Article
- Tonantzitlolone cytotoxicity toward renal cancer cells is PKCθ- and HSF1-dependent.Oncotarget · 2015Article
- Article
- Targeting ABL1-mediated oxidative stress adaptation in fumarate hydratase-deficient cancer.Cancer cell · 2014Article
- Molecular pathways: Fumarate hydratase-deficient kidney cancer--targeting the Warburg effect in cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013Review
- Article
- Identification of NCF2/p67phox as a novel p53 target gene.Cell cycle (Georgetown, Tex.) · 2012Article
- Hereditary leiomyomatosis and renal cell cancer: update on clinical and molecular characteristics.Familial cancer · 2011Article
- A novel fumarate hydratase-deficient HLRCC kidney cancer cell line, UOK268: a model of the Warburg effect in cancer.Cancer geneticsArticle
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Hereditary leiomyomatosis renal cell carcinoma (HLRCC)-associated renal tumors are aggressive and tend to metastasize early. There are currently no effective forms of therapy for patients with advanced HLRCC-associated kidney cancer. We have previously shown that HLRCC cells express a high level of reactive oxygen species (ROS). In the present study we investigated the cytotoxic effects of increasing ROS level using bortezomib in combination with cisplatin on HLRCC cells in vitro and in an in vivo xenograft model. The cytotoxic effect of several ROS inducers on FH-deficient cells was assessed by synthetic lethality. ROS inducers had a pronounced impact on the viability of FH-deficient cells. Because of its high potency, the proteasome inhibitor bortezomib was further investigated. Bortezomib induced apoptosis in vitro in HLRCC cells and inhibited HLRCC tumour growth in vivo. Bortezomib-associated cytotoxicity was highly correlated with cellular ROS level: combining bortezomib with other ROS inducers enhanced cytotoxicity, while combining bortezomib with a ROS scavenger inhibited its cytotoxic effect. Finally, HLRCC murine xenografts were treated with bortezomib and cisplatin, another ROS inducer. This regimen induced HLRCC tumour regression in vivo. These findings suggest that increasing ROS level in HLRCC above a certain threshold can induce HLRCC-tumor cell death. Increasing tumor ROS with bortezomib in combination with cisplatin represents a novel targeted therapeutic approach to treat advanced HLRCC-associated renal tumors.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.