ArticleInflammation and regeneration2020
Migration arrest of chemoresistant leukemia cells mediated by MRTF-SRF pathway.
Article in Inflammation and regeneration, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Dual-functional Nanocarrier for Improved Immunochemotherapy of Acute Myeloid Leukemia.Research square · 2026Article
- RHOA at the intersection of inflammation-driven and sporadic colorectal cancer.Frontiers in immunology · 2026Review
- The Role of Epithelial-to-Mesenchymal Transition Transcription Factors (EMT-TFs) in Acute Myeloid Leukemia Progression.Biomedicines · 2024Review
- Prediction of miRNA‑mRNA network regulating the migration ability of cytarabine‑resistant HL60 cells.Biomedical reports · 2024Article
- In vivo imaging of inflammatory response in cancer research.Inflammation and regeneration · 2023Review
- Multiphoton intravital microscopy of rodents.Nature reviews. Methods primers · 2022Article
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Authors and funding
9 authors at 2 institutions in 1 country.
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Abstract
backgroundDormant chemotherapy-resistant leukemia cells can survive for an extended period before relapse. Nevertheless, the mechanisms underlying the development of chemoresistance in vivo remain unclear.
methodsUsing intravital bone imaging, we characterized the behavior of murine acute myeloid leukemia (AML) cells (C1498) in the bone marrow before and after chemotherapy with cytarabine.
resultsProliferative C1498 cells exhibited high motility in the bone marrow. Cytarabine treatment impaired the motility of residual C1498 cells. However, C1498 cells regained their migration potential after relapse. RNA sequencing revealed that cytarabine treatment promoted MRTF-SRF pathway activation. MRTF inhibition using CCG-203971 augmented the anti-tumor effects of chemotherapy in our AML mouse model, as well as suppressed the migration of chemoresistant C1498 cells.
conclusionsThese results provide novel insight into the role of cell migration arrest on the development of chemoresistance in AML, as well as provide a strong rationale for the modulation of cellular motility as a therapeutic target for refractory AML.
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