ArticleMedical oncology (Northwood, London, England)2011
Knockdown of SOD1 sensitizes the CD34+ CML cells to imatinib therapy.
Article in Medical oncology (Northwood, London, England), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- BCAT1 contributes to the development of TKI-resistant CML.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- Exposure of chronic myelogenous leukemia cells to imatinib results in the post-transcriptional induction of manganese superoxide dismutase.Leukemia & lymphoma · 2015Article
- Mitochondrial membrane potential and reactive oxygen species in cancer stem cells.Familial cancer · 2015Review
- Manganese superoxide dismutase in cancer prevention.Antioxidants & redox signaling · 2014Review
- Quantitative phenotyping-based in vivo chemical screening in a zebrafish model of leukemia stem cell xenotransplantation.PloS one · 2014Article
- Overcoming challenges of ovarian cancer stem cells: novel therapeutic approaches.Stem cell reviews and reports · 2012Review
- miR-153 sensitized the K562 cells to As2O3-induced apoptosis.Medical oncology (Northwood, London, England) · 2012Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Leukemia stem cell is thought to be one of the leading causes of imatinib resistance and the resultant relapse of chronic myelogenous leukemia (CML). Eradicating the leukemia stem cells holds the promise of CML treatment. In this study, we found that the CD34+ subpopulation in the CML cell line K562 had a higher expression of SOD1 than that in the CD34 negative cells. Knockdown of SOD1 in CD34+ cells had no significant effects on cell survival and growth, while it sensitized the CD34+ cells to imatinib therapy. N-acetyl-L cysteine (NAC) blocked the pro-apoptotic effects of SOD1 knockdown, suggesting the antioxidant effects of SOD1 was essential for the resistance of CD34+ cells to imatinib therapy. In summary, our results suggest that antagonizing the enhanced endogenous antioxidant activity in leukemia stem cells sheds lights on CML therapy.
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Registered trials
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