ArticleOncotarget2017
Translocation of heme oxygenase-1 contributes to imatinib resistance in chronic myelogenous leukemia.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Transcriptional readthrough precedes alternative splicing programs triggered in CML cells by imatinib.Science advances · 2026Article
- HO-1-driven drug resistance in hematological malignancies: Mechanistic insights and advances in targeted therapy.iScience · 2026Review
- Gasotransmitters bridging tumor biology and immunity: from pathophysiological insights to therapeutic potential.Frontiers in immunology · 2026Review
- Predictive and prognostic effect of HO-1 expression in breast cancer patients undergoing neoadjuvant chemotherapy.Breast cancer research and treatment · 2022Article
- Review
- The Diverse Roles of Heme Oxygenase-1 in Tumor Progression.Frontiers in immunology · 2021Review
- Heme Oxygenase-1 Inhibition Sensitizes Human Prostate Cancer Cells towards Glucose Deprivation and Metformin-Mediated Cell Death.International journal of molecular sciences · 2019Article
- Insights into the mechanism of isoenzyme-specific signal peptide peptidase-mediated translocation of heme oxygenase.PloS one · 2017Article
Corrections and comments
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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
Heme oxygenase-1 (HO-1) degrades heme to bilirubin. In addition, it is upregulated in malignant disease and has been described as an important factor for cancer prognosis and therapy. Under physiological conditions HO-1 is anchored to the endoplasmic reticulum (ER). Under stress conditions HO-1 can be cleaved and subsequently translocates to the cytosol and nucleus. In this study we systematically investigated the influence of HO-1's catabolic activity and subcellular localization on resistance against the tyrosine kinase inhibitor imatinib in leukemia cells by confocal laser scanning microscopy, hemoglobin synthesis experiments and cell viability assays. We created two types of monoclonal K562 cell lines stably transfected with GFP-tagged HO-1: cell lines expressing ER anchored HO-1 or anchorless HO-1. Since translocation of HO-1 disrupts the association with cytochrome P450 reductase, heme degrading activity was higher for ER anchored versus anchorless HO-1. Cell viability tests with increasing concentrations of imatinib showed IC50-values for all six cell lines with ER localized HO-1 that were similar to control cells. However, out of the seven cell lines with anchorless HO-1, two showed a statistically significant increase in the imatinib IC50 (19.76 μM and 12.35 μM versus 2.35 - 7.57 μM of sensitive cell lines) corresponding to plasma concentrations outside the therapeutic range. We conclude that the presence of translocated HO-1 in the cytosol and nucleus supports imatinib resistance while it is not sufficient to cause imatinib resistance in every cell line. In contrast, an increase in ER anchored HO-1 with high heme degrading activity does not contribute to imatinib resistance.
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