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Inhibition of endogenous hydrogen sulfide production in clear-cell renal cell carcinoma cell lines and xenografts restricts their growth, survival and angiogenic potential. | LitMetric
Matthew Mailing Centre for Translational Transplant Studies, 339 Windermere Rd., London Health Sciences Centre, London, Ontario N6A 5A5, Canada; Department of Surgery, Schulich Medicine and Dentistry, 268 Grosvenor St., St Joseph's Hospital, London, Ontario N6A 4V2, Canada; Department of Microbiology and Immunology, Schulich Medicine and Dentistry, Dental Sciences Building Room 3014, Western University, London, Ontario N6A 5C1, Canada; Schulich School of Medicine and Dentistry, Clinical Skills Building, Western University, London, Ontario N6A 5C1, Canada; Multiorgan Transplant Program, 339 Windermere Rd., London Health Sciences Centre, London, Ontario N6A 5A5, Canada. Electronic address:
Published: September 2015
AI Article Synopsis
Article Abstract
Clear cell renal cell carcinoma (ccRCC) is characterized by Von Hippel-Lindau (VHL)-deficiency, resulting in pseudohypoxic, angiogenic and glycolytic tumours. Hydrogen sulfide (H2S) is an endogenously-produced gasotransmitter that accumulates under hypoxia and has been shown to be pro-angiogenic and cytoprotective in cancer. It was hypothesized that H2S levels are elevated in VHL-deficient ccRCC, contributing to survival, metabolism and angiogenesis. Using the H2S-specific probe MeRhoAz, it was found that H2S levels were higher in VHL-deficient ccRCC cell lines compared to cells with wild-type VHL. Inhibition of H2S-producing enzymes could reduce the proliferation, metabolism and survival of ccRCC cell lines, as determined by live-cell imaging, XTT/ATP assay, and flow cytometry respectively. Using the chorioallantoic membrane angiogenesis model, it was found that systemic inhibition of endogenous H2S production was able to decrease vascularization of VHL-deficient ccRCC xenografts. Endogenous H2S production is an attractive new target in ccRCC due to its involvement in multiple aspects of disease.
