ArticleOncotarget2018
Doxorubicin-induced loss of DNA topoisomerase II and DNMT1- dependent suppression of MiR-125b induces chemoresistance in ALK-positive cells.
Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- CircZBTB46, a promising therapeutic target in crizotinib resistant ALK-positive T lymphomas.Leukemia · 2026Article
- CircRNAs derived from the tyrosine phosphatase PTPN22 impact chemosensitivity in ALK-positive T-cell lymphomas.Scientific reports · 2026Article
- A Comprehensive Review on LncRNAs/miRNAs-DNMT1 Axis in Human Cancer: Mechanistic and Clinical Application.Journal of cellular and molecular medicine · 2025Review
- Modulatory effects of miRNAs in doxorubicin resistance: A mechanistic view.Functional & integrative genomics · 2024Review
- A review of the pathophysiological mechanisms of doxorubicin-induced cardiotoxicity and aging.npj aging · 2024Review
- MiR-125b targeted regulation of MKNK2 inhibits multiple myeloma proliferation and invasion.American journal of translational research · 2024Article
- From circRNAs to fusion circRNAs in hematological malignancies.JCI insight · 2021Review
- Personalized medicine of non-gene-specific chemotherapies for non-small cell lung cancer.Acta pharmaceutica Sinica. B · 2021Review
- Essential functions of miR-125b in cancer.Cell proliferation · 2021Review
- Review
- ALK-transformed mature T lymphocytes restore early thymus progenitor features.The Journal of clinical investigation · 2020Article
- Non-Coding RNA Networks in ALK-Positive Anaplastic-Large Cell Lymphoma.International journal of molecular sciences · 2019Review
- miR-497 suppresses cycle progression through an axis involving CDK6 in ALK-positive cells.Haematologica · 2019Article
- MiRNA Dysregulation in Childhood Hematological Cancer.International journal of molecular sciences · 2018Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Systemic anaplastic large-cell lymphoma (ALCL) is a childhood T cell neoplasm defined by the presence or absence of translocations that lead to the ectopic expression of anaplastic lymphoma kinase (ALK), with nucleophosmin-ALK (NPM-ALK) fusions being the most common. Polychemotherapy involving doxorubicin is the standard first-line treatment but for the 25 to 35% of patients who relapse and develop resistance the prognosis remains poor. We studied the potential role of the microRNA miR-125b in the development of resistance to doxorubicin in NPM-ALK(+) ALCL. Our results show that miR-125b expression is repressed in NPM-ALK(+) cell lines and patient samples through hypermethylation of its promoter. NPM-ALK activity, in cooperation with DNA topoisomerase II (Topo II) and DNA methyltransferase 1 (DNMT1), is responsible for miR-125b repression through DNA hypermethylation. MiR-125b repression was reversed by the inhibition of DNMTs with decitabine or the inhibition of DNA topoisomerase II with either doxorubicin or etoposide. In NPM-ALK(+) cell lines, doxorubicin treatment led to an increase in miR-125b levels by inhibiting the binding of DNMT1 to the
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