ArticleOncoTargets and therapy2020
The CXCR4 Antagonist, AMD3100, Reverses Mesenchymal Stem Cell-Mediated Drug Resistance in Relapsed/Refractory Acute Lymphoblastic Leukemia.
Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 30 citations in OpenAlex.
- CXCR4/CXCL12 blockade therapy; a new horizon in TNBC therapy.Medical oncology (Northwood, London, England) · 2025Review
- Review
- Molecular and cellular mechanisms of chemoresistance in paediatric pre-B cell acute lymphoblastic leukaemia.Cancer metastasis reviews · 2024Review
- Improving targeted small molecule drugs to overcome chemotherapy resistance.Cancer reports (Hoboken, N.J.) · 2024Review
- BM-MSCs display altered gene expression profiles in B-cell acute lymphoblastic leukemia niches and exert pro-proliferative effects via overexpression of IFI6.Journal of translational medicine · 2023Article
- Review
- Article
- Targeting chemokines for acute lymphoblastic leukemia therapy.Journal of hematology & oncology · 2021Review
- CXCR4 Mediates Enhanced Cell Migration inFrontiers in oncology · 2021Article
- The Role of Tumor-Stroma Interactions in Drug Resistance Within Tumor Microenvironment.Frontiers in cell and developmental biology · 2021Review
- Mesenchymal Stem Cells With Cancer-Associated Fibroblast-Like Phenotype Stimulate SDF-1/CXCR4 Axis to Enhance the Growth and Invasion of B-Cell Acute Lymphoblastic Leukemia Cells Through Cell-to-Cell Communication.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTo investigate the role of the CXCR4/CXCL12 axis in chemotherapy resistance in refractory/relapsed (R/R) ALL patients.
methodsCXCR4 expression on ALL cells from newly diagnosed or R/R ALL patients were detected using flow cytometry. The CXCR4/CXCL12 signaling pathway was blocked by the CXCR4 inhibitor AMD3100 in a co-culture model of primary drug-resistant ALL cells and umbilical cord mesenchymal stem cells (UCMSCs). Surface CXCR4 expression, apoptosis rate, and apoptosis-related protein expression in primary ALL cells under various treatments were detected.
resultsOf the 37 ALL patients examined, CXCR4 expression was higher in R/R patients than that in those with newly diagnosed disease. Similarly, in in vitro co-cultures of drug-resistant ALL cells with UCMSCs, the expression of CXCR4 was increased in the presence of vincristine (VCR), but reduced when VCR was combined with the CXCR4 antagonist AMD3100. Additionally, the supernatants of ALL-UCMSC co-cultures contained high CXCL12 concentrations, which were upregulated by VCR and significantly decreased by the combination of VCR plus AMD3100. Furthermore, the apoptosis rate of ALL cells significantly decreased, Bax expression was downregulated, and Bcl-2 was upregulated when ALL was co-cultured with UCMSCs compared with ALL cells alone. With the addition of VCR, the apoptosis rate mildly increased, Bax was upregulated, and Bcl-2 was downregulated. Nevertheless, the above results were further intensified, particularly Bax expression, when VCR was combined with AMD3100.
conclusionThe CXCR4 antagonist could effectively reverse MSC-mediated drug resistance by blocking the CXCR4/CXCL12 axis and sensitizing leukemic cells from R/R ALL patients to chemotherapy drugs.
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