ArticleOncotarget2015
Targeting SOD1 induces synthetic lethal killing in BLM- and CHEK2-deficient colorectal cancer cells.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
32 citing papers in PubMed, 44 citations in OpenAlex.
- Tumor CTR1 Expression and Systemic Copper Dynamics Converge on a Copper Axis in High-Grade Triple-Negative Breast Cancer.Cancer research communications · 2026Article
- Integrating machine learning and single-cell sequencing to reveal the role of kinase-related genes in subtype classification and prognostic significance of lung squamous cell carcinoma.Discover oncology · 2026Article
- Proteomic remodeling during tumor cell-induced platelet aggregation unveils metastatic drivers in colorectal cancer.Cancer cell international · 2026Article
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- Alpha-synuclein expression in neurons modulates Japanese encephalitis virus infection.Journal of virology · 2024Article
- The SOD1 Inhibitor, LCS-1, Oxidizes H2S to Reactive Sulfur Species, Directly and Indirectly, through Conversion of SOD1 to an Oxidase.Antioxidants (Basel, Switzerland) · 2024Article
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- Mitochondrial superoxide dismutase Sod2 suppresses nuclear genome instability during oxidative stress.Genetics · 2023Article
- Oxidative Stress Inducers in Cancer Therapy: Preclinical and Clinical Evidence.Antioxidants (Basel, Switzerland) · 2023Review
- Spermidine/Spermine N1-Acetyltransferase 1 (Cancers · 2022Article
- Non-Productive Infection of Glial Cells with SARS-CoV-2 in Hamster Organotypic Cerebellar Slice Cultures.Viruses · 2022Article
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- LCS-1 inhibition of superoxide dismutase 1 induces ROS-dependent death of glioma cells and degradates PARP and BRCA1.Frontiers in oncology · 2022Article
- Copper metabolism as a unique vulnerability in cancer.Biochimica et biophysica acta. Molecular cell research · 2021Review
- Synthetic Lethal Interactions of RECQ Helicases.Trends in cancer · 2021Review
- Exploring Candidate Human Synthetic Lethal Interactions Through siRNA and Quantitative Imaging-Based Approaches.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Employing Cross-Species Approaches to Construct Humanized Genetic Interaction Networks.Methods in molecular biology (Clifton, N.J.) · 2021Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Cancer is a major cause of death throughout the world, and there is a large need for better and more personalized approaches to combat the disease. Over the past decade, synthetic lethal approaches have been developed that are designed to exploit the aberrant molecular origins (i.e. defective genes) that underlie tumorigenesis. BLM and CHEK2 are two evolutionarily conserved genes that are somatically altered in a number of tumor types. Both proteins normally function in preserving genome stability through facilitating the accurate repair of DNA double strand breaks. Thus, uncovering synthetic lethal interactors of BLM and CHEK2 will identify novel candidate drug targets and lead chemical compounds. Here we identify an evolutionarily conserved synthetic lethal interaction between SOD1 and both BLM and CHEK2 in two distinct cell models. Using quantitative imaging microscopy, real-time cellular analyses, colony formation and tumor spheroid models we show that SOD1 silencing and inhibition (ATTM and LCS-1 treatments), or the induction of reactive oxygen species (2ME2 treatment) induces selective killing within BLM- and CHEK2-deficient cells relative to controls. We further show that increases in reactive oxygen species follow SOD1 silencing and inhibition that are associated with the persistence of DNA double strand breaks, and increases in apoptosis. Collectively, these data identify SOD1 as a novel candidate drug target in BLM and CHEK2 cancer contexts, and further suggest that 2ME2, ATTM and LCS-1 are lead therapeutic compounds warranting further pre-clinical study.
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What OpenQuestion holds
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.