ArticleMolecular neurobiology2020
Heme Oxygenase-1 and Carbon Monoxide Regulate Growth and Progression in Glioblastoma Cells.
Article in Molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- Plasma proteomic biomarkers predict therapeutic responses in advanced biliary tract cancer patients receiving Camrelizumab plus the GEMOX treatment.NPJ precision oncology · 2025Article
- Ferroptosis-Related Transcriptional Level Changes and the Role of CIRBP in Glioblastoma Cells Ferroptosis.Biomedicines · 2024Article
- Unveiling the Molecular Mechanisms of Glioblastoma through an Integrated Network-Based Approach.Biomedicines · 2024Article
- Novel Acetamide-Based HO-1 Inhibitor Counteracts Glioblastoma Progression by Interfering with the Hypoxic-Angiogenic Pathway.International journal of molecular sciences · 2024Article
- The Interplay between Glioblastoma Cells and Tumor Microenvironment: New Perspectives for Early Diagnosis and Targeted Cancer Therapy.Brain sciences · 2024Review
- 1,4-dihydroxy quininib activates ferroptosis pathways in metastatic uveal melanoma and reveals a novel prognostic biomarker signature.Cell death discovery · 2024Article
- Heme catabolism and heme oxygenase-1-expressing myeloid cells in pathophysiology.Frontiers in immunology · 2024Review
- Bradykinin B1 Receptor Affects Tumor-Associated Macrophage Activity and Glioblastoma Progression.Antioxidants (Basel, Switzerland) · 2023Article
- Article
- Pyroptosis, ferroptosis, and autophagy cross-talk in glioblastoma opens up new avenues for glioblastoma treatment.Cell communication and signaling : CCS · 2023Review
- Soluble peptidoglycan fragments produced byFrontiers in molecular biosciences · 2023Article
- Heme Oxygenase-1 Overexpression Promotes Uveal Melanoma Progression and Is Associated with Poor Clinical Outcomes.Antioxidants (Basel, Switzerland) · 2022Article
- Adaptive Changes Allow Targeting of Ferroptosis for Glioma Treatment.Cellular and molecular neurobiology · 2022Review
- Head-to-Head Comparison of Selected Extra- and Intracellular CO-Releasing Molecules on Their CO-Releasing and Anti-Inflammatory Properties.Chembiochem : a European journal of chemical biology · 2022Article
- Expression Dynamics of Heme Oxygenase-1 in Tumor Cells and the Host Contributes to the Progression of Tumors.Journal of personalized medicine · 2021Article
- A Novel Class of Dual-Acting DCH-CORMs Counteracts Oxidative Stress-Induced Inflammation in Human Primary Tenocytes.Antioxidants (Basel, Switzerland) · 2021Article
- Discovery of Novel Acetamide-Based Heme Oxygenase-1 Inhibitors with PotentJournal of medicinal chemistry · 2021Article
- Review
- Combination of Heme Oxygenase-1 Inhibition and Sigma Receptor Modulation for Anticancer Activity.Molecules (Basel, Switzerland) · 2021Article
- Heme oxygenase 1: a novel oncogene in multiple gynecological cancers.International journal of biological sciences · 2021Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In human glioma tumours, heme oxygenase-1 (HO-1) is overexpressed when compared with normal brain tissues and during oligodendroglioma progression. However, the molecular mechanisms mediated by HO-1 to promote glioblastoma remain unknown. We therefore aimed at investigating the effect of HO-1 expression and its selective enzymatic inhibition in two different cell lines (i.e. A172 and U87-MG). HO-1 was induced by hemin treatment (10 μM), and VP13/47 (100 μM) was used as a specific non-competitive inhibitor of HO-1 activity. Cell proliferation was measured by cell index measurement (xCelligence technology) and clonogenic assay, whereas cell migration was assessed by wound healing assay. Carbon monoxide-releasing molecules (CORMs) (i.e. CORM-3 and CORM-A1) were also used in a separate set of experiments to confirm the effect of HO-1 by-product in glioblastoma progression further. Our results were further validated using GSE4412 microarray dataset analysis and comparing biopsies overexpressing HO-1 with the rest of the cases. Our results showed that hemin was able to induce both HO-1 gene and protein expression in a cell-dependent manner being A172 more responsive to pharmacological upregulation of HO-1. Hemin, but not CORMs treatment, resulted in a significant increase of cell proliferation following 24 h of treatment as measured by increased cell index and colony formation capacity and such effect was abolished by VP13/47. Interestingly, both hemin and CORMs showed a significant effect on the wound healing assay also exhibiting cell specificity. Finally, our dataset analysis showed a positive correlation of HO-1 gene expression with ITGBI and ITGBII which are membrane receptors involved in cell adhesion, embryogenesis, tissue repair, immune response and metastatic diffusion of tumour cells. In conclusion, our data suggest that HO-1 and its by-product CO exhibit a cell-specific effect on various aspects of disease progression and are associated with a complex series of molecular mechanisms driving cell proliferation, survival and metastasis.
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