ArticleThe Journal of biological chemistry2012
Carbon monoxide mediates the anti-apoptotic effects of heme oxygenase-1 in medulloblastoma DAOY cells via K+ channel inhibition.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 62 citations in OpenAlex.
- Gasotransmitters bridging tumor biology and immunity: from pathophysiological insights to therapeutic potential.Frontiers in immunology · 2026Review
- The Triple Crown: NO, CO, and HPharmacology & therapeutics · 2023Review
- Potassium Channels, Glucose Metabolism and Glycosylation in Cancer Cells.International journal of molecular sciences · 2023Review
- Antagonistic roles of Ras-MAPK and Akt signaling in integrin-KFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Non-canonical vs. Canonical Functions of Heme Oxygenase-1 in Cancer.Journal of cancer prevention · 2022Review
- WD-40 repeat protein 26 protects against oxidative stress-induced injury in astrocytes via Nrf2/HO-1 pathways.Molecular biology reports · 2022Article
- Review
- Hydrogen sulfide regulates hippocampal neuron excitability via S-sulfhydration of Kv2.1.Scientific reports · 2021Article
- Heme Oxygenase-1 as a Pharmacological Target for Host-Directed Therapy to Limit Tuberculosis Associated Immunopathology.Antioxidants (Basel, Switzerland) · 2021Review
- The Diverse Roles of Heme Oxygenase-1 in Tumor Progression.Frontiers in immunology · 2021Review
- Tyrosine Phosphorylation of the KInternational journal of molecular sciences · 2020Article
- Effects of curcumin complexes on MDA‑MB‑231 breast cancer cell proliferation.International journal of oncology · 2020Article
- Heme Oxygenase-1 in Central Nervous System Malignancies.Journal of clinical medicine · 2020Review
- Identification of Hub Genes in Pediatric Medulloblastoma by Multiple-Microarray Analysis.Journal of molecular neuroscience : MN · 2020Article
- Identification of a Twelve-Gene Signature and Establishment of a Prognostic Nomogram Predicting Overall Survival for Medulloblastoma.Frontiers in genetics · 2020Article
- Voltage-Gated Potassium Channels as Regulators of Cell Death.Frontiers in cell and developmental biology · 2020Review
- Review
- Article
- Heme oxygenase-1 derived carbon monoxide suppresses AβCell death & disease · 2017Article
- Oxidation of KCNB1 potassium channels triggers apoptotic integrin signaling in the brain.Cell death & disease · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Tumor cell survival and proliferation is attributable in part to suppression of apoptotic pathways, yet the mechanisms by which cancer cells resist apoptosis are not fully understood. Many cancer cells constitutively express heme oxygenase-1 (HO-1), which catabolizes heme to generate biliverdin, Fe(2+), and carbon monoxide (CO). These breakdown products may play a role in the ability of cancer cells to suppress apoptotic signals. K(+) channels also play a crucial role in apoptosis, permitting K(+) efflux which is required to initiate caspase activation. Here, we demonstrate that HO-1 is constitutively expressed in human medulloblastoma tissue, and can be induced in the medulloblastoma cell line DAOY either chemically or by hypoxia. Induction of HO-1 markedly increases the resistance of DAOY cells to oxidant-induced apoptosis. This effect was mimicked by exogenous application of the heme degradation product CO. Furthermore we demonstrate the presence of the pro-apoptotic K(+) channel, Kv2.1, in both human medulloblastoma tissue and DAOY cells. CO inhibited the voltage-gated K(+) currents in DAOY cells, and largely reversed the oxidant-induced increase in K(+) channel activity. p38 MAPK inhibition prevented the oxidant-induced increase of K(+) channel activity in DAOY cells, and enhanced their resistance to apoptosis. Our findings suggest that CO-mediated inhibition of K(+) channels represents an important mechanism by which HO-1 can increase the resistance to apoptosis of medulloblastoma cells, and support the idea that HO-1 inhibition may enhance the effectiveness of current chemo- and radiotherapies.
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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.