Part of: Cancer Cell Line Encyclopedia (CCLE) project.
Part of: JFCR39 cancer cell line panel.
Part of: KuDOS 95 cell line panel.
Part of: MD Anderson Cell Lines Project.
Part of: NCI60 cancer cell line panel.
Doubling time: 38 hours (in RPMI 1640+10% FBS), 71 hours (in ACL-3), 57 hours (in ACL-3+BSA) (PubMed=3940644); 35 hours (PubMed=25984343); 33.4 hours (NCI-DTP).
Microsatellite instability: Stable (MSS) (Sanger).
Omics: Deep exome analysis.
Omics: Deep phosphoproteome analysis.
Omics: Deep proteome analysis.
Omics: Deep RNAseq analysis.
Omics: DNA methylation analysis.
Omics: Fluorescence phenotype profiling.
Omics: lncRNA expression profiling.
Omics: Metabolome analysis.
Omics: Protein expression by reverse-phase protein arrays.
Omics: shRNA library screening.
Omics: SNP array analysis.
Omics: Transcriptome analysis.
Misspelling: 'H23' in PubMed=23381221 and PubMed=25120651 (confirmed by author personal communication).
Literature context: ollection RRID:CVCL_1547
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.
Many lines of evidence have indicated that both genetic and non-genetic determinants can contribute to intra-tumor heterogeneity and influence cancer outcomes. Among the best described sub-population of cancer cells generated by non-genetic mechanisms are cells characterized by a CD44+/CD24- cell surface marker profile. Here, we report that human CD44+/CD24- cancer cells are genetically highly unstable because of intrinsic defects in their DNA-repair capabilities. In fact, in CD44+/CD24- cells, constitutive activation of the TGF-beta axis was both necessary and sufficient to reduce the expression of genes that are crucial in coordinating DNA damage repair mechanisms. Consequently, we observed that cancer cells that reside in a CD44+/CD24- state are characterized by increased accumulation of DNA copy number alterations, greater genetic diversity and improved adaptability to drug treatment. Together, these data suggest that the transition into a CD44+/CD24- cell state can promote intra-tumor genetic heterogeneity, spur tumor evolution and increase tumor fitness.
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