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O2⋅- and H2O2-Mediated Disruption of Fe Metabolism Causes the Differential Susceptibility of NSCLC and GBM Cancer Cells to Pharmacological Ascorbate.

Cancer cell | Apr 10, 2017

Pharmacological ascorbate has been proposed as a potential anti-cancer agent when combined with radiation and chemotherapy. The anti-cancer effects of ascorbate are hypothesized to involve the autoxidation of ascorbate leading to increased steady-state levels of H2O2; however, the mechanism(s) for cancer cell-selective toxicity remain unknown. The current study shows that alterations in cancer cell mitochondrial oxidative metabolism resulting in increased levels of O2⋅- and H2O2 are capable of disrupting intracellular iron metabolism, thereby selectively sensitizing non-small-cell lung cancer (NSCLC) and glioblastoma (GBM) cells to ascorbate through pro-oxidant chemistry involving redox-active labile iron and H2O2. In addition, preclinical studies and clinical trials demonstrate the feasibility, selective toxicity, tolerability, and potential efficacy of pharmacological ascorbate in GBM and NSCLC therapy.

Pubmed ID: 28366679 RIS Download

Mesh terms: Animals | Antineoplastic Combined Chemotherapy Protocols | Ascorbic Acid | Brain Neoplasms | Carcinoma, Non-Small-Cell Lung | Cell Line, Tumor | Chemoradiotherapy | Female | Glioblastoma | Humans | Hydrogen Peroxide | Iron | Lung Neoplasms | Male | Mice, Nude | Oxygen | Radiation-Sensitizing Agents | Xenograft Model Antitumor Assays

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Associated grants

  • Agency: NCI NIH HHS, Id: R01 CA184051
  • Agency: NCI NIH HHS, Id: U01 CA140206
  • Agency: NIEHS NIH HHS, Id: P30 ES005605
  • Agency: NCI NIH HHS, Id: U01 CA166800
  • Agency: NCI NIH HHS, Id: P30 CA086862
  • Agency: NCI NIH HHS, Id: R01 CA169046
  • Agency: NCI NIH HHS, Id: T32 CA078586
  • Agency: NCI NIH HHS, Id: R01 CA182804
  • Agency: NIGMS NIH HHS, Id: T32 GM007337

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