ArticleCancer cell international2018
Catalase down-regulation in cancer cells exposed to arsenic trioxide is involved in their increased sensitivity to a pro-oxidant treatment.
Article in Cancer cell international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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26 citing papers in PubMed, 56 citations in OpenAlex.
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- Catalase: The golden key to regulate oxidative stress in breast cancer.World journal of clinical oncology · 2025Review
- Curcumin-piperine nanoparticles mitigate cuprizone-induced cognitive impairment via antioxidant and anti-inflammatory mechanisms.Frontiers in nutrition · 2025Article
- The role of mitochondrial dysfunction in the cytotoxic synergistic effect of gemcitabine and arsenic on breast cancer.PloS one · 2025Article
- Targeting catalase in cancer.Redox biology · 2024Review
- Several lines of antioxidant defense against oxidative stress: antioxidant enzymes, nanomaterials with multiple enzyme-mimicking activities, and low-molecular-weight antioxidants.Archives of toxicology · 2024Review
- Excavatolide C/cisplatin combination induces antiproliferation and drives apoptosis and DNA damage in bladder cancer cells.Archives of toxicology · 2024Article
- The Multifaceted Roles of NRF2 in Cancer: Friend or Foe?Antioxidants (Basel, Switzerland) · 2024Review
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- The Effect of Encapsulated Apigenin Nanoparticles on HePG-2 Cells through Regulation of P53.Pharmaceutics · 2022Article
- Targeting of the intracellular redox balance by metal complexes towards anticancer therapy.Frontiers in chemistry · 2022Review
- Singlet Oxygen, Photodynamic Therapy, and Mechanisms of Cancer Cell Death.Journal of oncology · 2022Review
- Comparative Proteomics Analysis Reveals the Reversal Effect of Cryptotanshinone on Gefitinib-Resistant Cells in Epidermal Growth Factor Receptor-Mutant Lung Cancer.Frontiers in pharmacology · 2022Article
- Differential Expression of Peroxisomal Proteins in Distinct Types of Parotid Gland Tumors.International journal of molecular sciences · 2021Article
- Metabolomic Identification of Anticancer Metabolites of Australian Propolis and Proteomic Elucidation of Its Synergistic Mechanisms with Doxorubicin in the MCF7 Cells.International journal of molecular sciences · 2021Article
- Plant catalases as NO and HRedox biology · 2020Review
- Targeting the Redox Landscape in Cancer Therapy.Cancers · 2020Review
- Antioxidant defence barrier of great tit Parus major nestlings in response to trace elements.Environmental science and pollution research international · 2020Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPro-oxidant drugs have been proposed for treating certain cancers but the resistance developed by cancer cells to oxidative stress limits its potential use in clinics. To understand the mechanisms underlying resistance to oxidative stress, we found that the chronic exposure to an H
methodsModulation of catalase expression was performed by either protein overexpression or protein down-regulation using siRNA against catalase and aminotriazole as pharmacological inhibitor. The former approach was done by transfecting cells with a plasmid construct containing human catalase cDNA (CAT3 cells, derived from MCF-7 breast cancer cell line) or by generating resistant cells through chronic exposure to an oxidant injury (Resox cells). Cell survival was monitored by using the MTT reduction assay and further calculation of IC
resultsUsing Resox and CAT3 cells (derived from MCF-7 breast cancer cell line) as models for cancer resistance to pro-oxidative treatment, we found that arsenic trioxide (ATO) remarkably sensitized Resox and CAT3 cells to Asc/Men treatment. Since catalase is a key antioxidant enzyme involved in detoxifying Asc/Men (as shown by siRNA-mediated catalase knockdown) that is overexpressed in resistant cells, we hypothesized that ATO might regulate the expression levels of catalase. Consistently, catalase protein level is decreased in Resox cells when incubated with ATO likely by a decreased transcriptional activity of the
conclusionsOur findings support the proposal that ATO should be administered in combination with pro-oxidant drugs to enhance cancer cell death in solid tumors.
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